研究者を探す
成石 浩司
2024年5月3日更新
- 職名
- 講師
- 電話
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- 電子メール
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- 学歴
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- 学位
- 博士 (歯学)
- 職歴・経歴
- 2014/4: 徳島大学 講師, 病院 (-2024.3.)
- 専門分野・研究分野
- 歯周病学
歯内療法学 (Endodontology)
2024年5月3日更新
- 専門分野・研究分野
- 歯周病学
歯内療法学 (Endodontology) - 担当経験のある授業科目
- (臨床系)国家試験・CBT対策講義 (学部)
保存系歯科学 (学部)
保存系歯科学(3年生Manaba用) (学部)
内分泌・代謝コース (学部)
歯周治療学各論 (学部)
歯周治療学実習 (学部)
歯周病学概論 (大学院)
歯科保存学(2) 実習 (学部)
歯科保存学(2)B 講義 (学部)
総合歯科学三 (学部)
臨床実習 (学部)
臨床実習(5年) (学部)
高齢者歯科学実験実習 (大学院) - 指導経験
- 研究者総覧に該当データはありませんでした。
2024年5月3日更新
- 専門分野・研究分野
- 歯周病学
歯内療法学 (Endodontology)
- 研究テーマ
- 歯周病における歯周組織細胞の作用
根尖性歯周炎の治癒メカニズム
- 著書
- Yuji Inagaki, Jun-ichi Kido, Yasufumi Nishikawa, Rie Kido, Eijiro Sakamoto, Mika Bandou, Koji Naruishi, Toshihiko Nagata and Hiromichi Yumoto :
Gan-Lu-Yin (Kanroin), Traditional Chinese Herbal Extracts, Reduces Osteoclast Differentiation In Vitro and Prevents Alveolar Bone Resorption in Rat Experimental Periodontitis,
Jul. 2021. 成石 浩司, 永田 俊彦 :
腎臓と他臓器連関を考える 臓器連関の実態 腎臓-口腔連関,
南江堂, 2020年8月. 成石 浩司, 永田 俊彦 :
ザ・ペリオドントロジー「歯周病と慢性腎臓病(CKD)」,
永末書店, 2019年2月. Timothy C Thompson, Saladihan A Tahir, Likun Li, Masami Watanabe, Koji Naruishi, Guang Yang and Ken-ichi Tabata :
Local and distant effects of caveolin-1 on prostate cancer tumor progression,
Springer Science + Business Media, Mar. 2011. Timme L Terry, Fujita Tetsuo, Wang Hongyu, Koji Naruishi, Kadmon Dov and Thompson C Timothy :
Cytokine Gene Therapy for Genitourinary Cancer,
The Humana Press, 2007. - 論文
- Jun-ichi Kido, Yuka Hiroshima, Rie Kido, Kaya Yoshida, Yuji Inagaki, Koji Naruishi, Kazuaki Kajimoto, Masatoshi Kataoka, Yasuo Shinohara and Hiromichi Yumoto :
Lipocalin 2, synthesized using a cell-free protein synthesis system and encapsulated into liposomes, inhibits the adhesion of Porphyromonas gingivalis to human oral epithelial cells.,
Journal of Periodontal Research, Vol.58, No.2, 262-273, 2023.- (徳島大学機関リポジトリ)
- ● Metadata: 119199
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1111/jre.13088
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36579753
- ● Search Scopus @ Elsevier (PMID): 36579753
- ● Search Scopus @ Elsevier (DOI): 10.1111/jre.13088
(徳島大学機関リポジトリ: 119199, DOI: 10.1111/jre.13088, PubMed: 36579753) Yasufumi Nishikawa, Yoritoki Tomotake, Hiromichi Kawano, Koji Naruishi, Jun-ichi Kido, Yuka Hiroshima, Akikazu Murakami, Tetsuo Ichikawa and Hiromichi Yumoto :
Effects of Candidalysin Derived from Candida albicans on the Expression of Pro-Inflammatory Mediators in Human Gingival Fibroblasts,
International Journal of Molecular Sciences, Vol.24, No.4, 3256, 2023.- (徳島大学機関リポジトリ)
- ● Metadata: 118834
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.3390/ijms24043256
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36834667
- ● Search Scopus @ Elsevier (PMID): 36834667
- ● Search Scopus @ Elsevier (DOI): 10.3390/ijms24043256
(徳島大学機関リポジトリ: 118834, DOI: 10.3390/ijms24043256, PubMed: 36834667) Koji Naruishi :
Biological Roles of Fibroblasts in Periodontal Diseases.,
Cells, Vol.11, No.21, 3345, 2022.- (要約)
- Periodontal diseases include periodontitis and gingival overgrowth. Periodontitis is a bacterial infectious disease, and its pathological cascade is regulated by many inflammatory cytokines secreted by immune or tissue cells, such as interleukin-6. In contrast, gingival overgrowth develops as a side effect of specific drugs, such as immunosuppressants, anticonvulsants, and calcium channel blockers. Human gingival fibroblasts (HGFs) are the most abundant cells in gingival connective tissue, and human periodontal ligament fibroblasts (HPLFs) are located between the teeth and alveolar bone. HGFs and HPLFs are both crucial for the remodeling and homeostasis of periodontal tissue, and their roles in the pathogenesis of periodontal diseases have been examined for 25 years. Various responses by HGFs or HPLFs contribute to the progression of periodontal diseases. This review summarizes the biological effects of HGFs and HPLFs on the pathogenesis of periodontal diseases.
- (徳島大学機関リポジトリ)
- ● Metadata: 117989
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.3390/cells11213345
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36359741
- ● Search Scopus @ Elsevier (PMID): 36359741
- ● Search Scopus @ Elsevier (DOI): 10.3390/cells11213345
(徳島大学機関リポジトリ: 117989, DOI: 10.3390/cells11213345, PubMed: 36359741) Koji Naruishi, Chie Wada -Mihara, Keiji Oishi and Toshihiko Nagata :
Dental students' awareness after clinical training between dental treatment and systemic health: A questionnaire-based survey,
Frontiers in Dental Medicine, 2022.- (出版サイトへのリンク)
- ● Publication site (DOI): 10.3389/fdmed.2021.740441
- (文献検索サイトへのリンク)
- ● Search Scopus @ Elsevier (DOI): 10.3389/fdmed.2021.740441
(DOI: 10.3389/fdmed.2021.740441) Yuji Inagaki, Jun-ichi Kido, Yasufumi Nishikawa, Rie Kido, Eijiro Sakamoto, Mika Bandou, Koji Naruishi, Toshihiko Nagata and Hiromichi Yumoto :
Gan-Lu-Yin (Kanroin), traditional Chinese herbal extracts, reduces osteoclast differentiation in vitro and prevents alveolar bone resorption in rat experimental periodontitis,
Journal of Clinical Medicine, Vol.10, No.3, 386, 2021.- (要約)
- Gan-Lu-Yin (GLY), a traditional Chinese herbal medicine, shows therapeutic effects on periodontitis, but that mechanism is not well known. This study aims to clarify the precise mechanism by investigating the inhibitory effects of GLY extracts on osteoclastogenesis in vitro and on bone resorption in periodontitis in vivo. RAW264.7 cells are cultured with soluble receptor activator of nuclear factor-kappa B (sRANKL) and GLY extracts (0.01-1.0 mg/mL), and stained for tartrate-resistant acid phosphatase (TRAP) to evaluate osteoclast differentiation. Experimental periodontitis is induced by placing a nylon ligature around the second maxillary molar in rats, and rats are administered GLY extracts (60 mg/kg) daily for 20 days. Their maxillae are collected on day 4 and 20, and the levels of alveolar bone resorption and osteoclast differentiation are estimated using micro-computed tomography (CT) and histological analysis, respectively. In RAW264.7 cells, GLY extracts significantly inhibit sRANKL-induced osteoclast differentiation at a concentration of more than 0.05 mg/mL. In experimental periodontitis, administering GLY extracts significantly decreases the number of TRAP-positive osteoclasts in the alveolar bone on day 4, and significantly inhibits the ligature-induced bone resorption on day 20. These results show that GLY extracts suppress bone resorption by inhibiting osteoclast differentiation in experimental periodontitis, suggesting that GLY extracts are potentially useful for oral care in periodontitis.
- (徳島大学機関リポジトリ)
- ● Metadata: 116745
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.3390/jcm10030386
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33498415
- ● Search Scopus @ Elsevier (PMID): 33498415
- ● Search Scopus @ Elsevier (DOI): 10.3390/jcm10030386
(徳島大学機関リポジトリ: 116745, DOI: 10.3390/jcm10030386, PubMed: 33498415) 西川 泰史, 成石 浩司, 木戸 淳一, 湯本 浩通 :
高グルコース条件下における歯肉線維芽細胞のカルプロテクチン誘導性炎症関連因子の産生におけるスダチチンの抑制効果,
日本歯科保存学雑誌, Vol.63, No.6, 503-511, 2020年.- (キーワード)
- 糖尿病 / 歯周病 / スダチチン / カルプロテクチン / 歯肉線維芽細胞 / diabetes mellitus / periodontitis / Sudachitin / calprotectin / gingival fibroblasts
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.11471/shikahozon.63.503
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390849931318242944
- ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.63.503
(DOI: 10.11471/shikahozon.63.503, CiNii: 1390849931318242944) Shotaroh Yoshioka, Takeshi Miyamoto, Junichiro Satomi, Yoshiteru Tada, Kenji Yagi, Kenji Shimada, Koji Naruishi, Eiji Shikata, Izumi Yamaguchi, Tadashi Yamaguchi, Masaaki Korai, Yoshihiro Okayama, Masafumi Harada, Keiko Kitazato, Yasuhisa Kanematsu, Shinji Nagahiro and Yasushi Takagi :
Disequilibrium of Plasma Protease/Anti-Protease Due to Severe Periodontal Disease Contributes to Human Subarachnoid Hemorrhage,
Neurosurgery Open, Vol.1, No.3, 1-9, 2020.- (徳島大学機関リポジトリ)
- ● Metadata: 115292
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1093/neuopn/okaa007
- (文献検索サイトへのリンク)
- ● Search Scopus @ Elsevier (DOI): 10.1093/neuopn/okaa007
(徳島大学機関リポジトリ: 115292, DOI: 10.1093/neuopn/okaa007) Rie Kido, Yuka Hiroshima, Jun-ichi Kido, Takahisa Ikuta, Eijiro Sakamoto, Yuji Inagaki, Koji Naruishi and Hiromichi Yumoto :
Advanced glycation end-products increase lipocalin 2 expression in human oral epithelial cells.,
Journal of Periodontal Research, Vol.55, No.4, 539-550, 2020.- (徳島大学機関リポジトリ)
- ● Metadata: 114681
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1111/jre.12741
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32170733
- ● Summary page in Scopus @ Elsevier: 2-s2.0-85081730917
(徳島大学機関リポジトリ: 114681, DOI: 10.1111/jre.12741, PubMed: 32170733, Elsevier: Scopus) 成石 浩司, 坂本 英次郎, 生田 貴久, 木戸 理恵, 木戸 淳一, 湯本 浩通 :
講義および実習試験の評価による歯周病学教育のあり方の考察,
日本歯科保存学雑誌, Vol.63, No.1, 22-29, 2020年.- (要約)
- <p> 目的 : 一般的に, 臨床実習前の歯学部生に対する歯周病学の教育は, 座学講義と基礎 (模型) 実習を主体とする. 本研究の目的は, 歯周病学の講義および実習の評価試験の結果の関連性を調べ, 将来の歯学部生に対する歯周病学教育のあり方について考察することである.</p><p> 方法 : 2018年度後期から2019年度前期に徳島大学歯学部に在籍し, 歯周病学を履修する歯学部3∼4年次生43名を対象とした. 歯周病学の講義前後に当該分野に関する筆記試験 (5肢2択形式) を行い, さらに歯周病学の基礎 (模型) 実習の終了時に, 顎模型を用いてスケーリング・ルートプレーニングの実習試験を行った. 講義による学生の理解度・習得度の評価は, カイ二乗検定を用いて判定した. 筆記試験および実習試験の結果の関連性は, スピアマンの順位相関検定を用いて判定した. また, 筆記試験の点数を25点満点で9点以下, 10∼12点, 13点以上の3群に分類し, 各群間の実習試験点数の差異の有無について, ANOVA-Tukey HSD解析を用いて判定した. なお, p値が0.05未満を有意差ありと判定した.</p><p> 結果 : 歯周病学の講義後の筆記試験の点数は, 出題内容によって差はあるものの, 講義前と比較しておおむね有意に上昇した. 筆記試験の結果と実技試験の結果は, 有意に相関した (r=0.34, p=0.025). また筆記試験の点数が9点以下の群における実習試験の点数は, 筆記試験の点数が10∼12点, 13点以上の群と比較して有意に低かった (p<0.05). 一方, 筆記試験の点数が10∼12点と13点以上の群間における実習試験の点数に有意差は認められなかった (p=0.76).</p><p> 結論 : 臨床実習前の歯周病学の学生教育において, 筆記試験の点数と基礎 (模型) 実習試験の点数は有意に相関した. このことは, 将来の効果的な歯周病学の教育システム構築の一助となる可能性を示唆する.</p>
- (キーワード)
- 歯学教育 / 歯周病学 / 基礎(模型)実習試験 / 筆記試験
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.11471/shikahozon.63.22
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390002184879112064
- ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.63.22
(DOI: 10.11471/shikahozon.63.22, CiNii: 1390002184879112064) Ryosuke Takagi, Eijiro Sakamoto, Jun-ichi Kido, Yuji Inagaki, Yuka Hiroshima, Koji Naruishi and Hiromichi Yumoto :
S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells.,
BioMed Research International, Vol.2020, No.7149408, 2020.- (徳島大学機関リポジトリ)
- ● Metadata: 114641
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1155/2020/7149408
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32149126
- ● Search Scopus @ Elsevier (PMID): 32149126
- ● Search Scopus @ Elsevier (DOI): 10.1155/2020/7149408
(徳島大学機関リポジトリ: 114641, DOI: 10.1155/2020/7149408, PubMed: 32149126) Masami Ninomiya, Mari Hashimoto, Kouji Yamanouchi, Yoshiaki Fukumura, Toshihiko Nagata and Koji Naruishi :
Relationship of oral conditions to the incidence of infective endocarditis in periodontitis patients with valvular heart disease: a cross-sectional study.,
Clinical Oral Investigations, Vol.24, No.2, 833-840, 2020.- (要約)
- No significant differences were observed between patients with or without VHD in oral conditions. A significant increase in the percentage of alveolar bone loss in VHD patients with IE was observed compared with that of patients without IE. The ratio of both Porphyromonas gingivalis (Pg) IgG titer > 1.68 and Pg fimA type II genotype in patients with IE was significantly higher than in patients without IE. There was a significant correlation between the occurrence of IE and clinical oral findings (number of remaining teeth: OR, 0.17; rate of alveolar bone loss > 40%: OR, 11.8).
- (キーワード)
- 感染性心内膜炎 / 心弁膜症 / 歯周病 (periodontitis)
- (徳島大学機関リポジトリ)
- ● Metadata: 113773
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1007/s00784-019-02973-2
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31197658
- ● Summary page in Scopus @ Elsevier: 2-s2.0-85067639107
(徳島大学機関リポジトリ: 113773, DOI: 10.1007/s00784-019-02973-2, PubMed: 31197658, Elsevier: Scopus) Koji Naruishi :
Carotenoids and Periodontal Infection.,
Nutrients, Vol.12, No.1, E269, 2020.- (要約)
- ) is associated with increased atherosclerosis, diabetes mellitus, and other systemic diseases through blood stream. On the other hand, carotenoids belong among phytochemicals that are responsible for different colors of the foods. It is important to examine whether carotenoids are effective to the inhibition of periodontal infection/inflammation cascades. This review summarizes the advanced state of knowledge about suppression of periodontal infection by several carotenoids. A series of findings suggest that carotenoids intake may provide novel strategy for periodontitis treatment, although further study will be needed.
- (徳島大学機関リポジトリ)
- ● Metadata: 115657
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.3390/nu12010269
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31968635
- ● Search Scopus @ Elsevier (PMID): 31968635
- ● Search Scopus @ Elsevier (DOI): 10.3390/nu12010269
(徳島大学機関リポジトリ: 115657, DOI: 10.3390/nu12010269, PubMed: 31968635) Kohei Nonaka, Mika Bandou, Eijiro Sakamoto, Yuji Inagaki, Koji Naruishi, Hiromichi Yumoto and Jun-ichi Kido :
6-Shogaol inhibits advanced glycation end-products-induced IL-6 and ICAM-1 expression by regulating oxidative responses in human gingival fibroblasts,
Molecules, Vol.24, No.20, e3705, 2019.- (要約)
- Advanced glycation end-products (AGEs) cause diabetes mellitus (DM) complications and accumulate more highly in periodontal tissues of patients with periodontitis and DM. AGEs aggravate periodontitis with DM by increasing the expression of inflammation-related factors in periodontal tissues. 6-Shogaol, a major compound in ginger, has anti-inflammatory and anti-oxidative activities. However, the influence of shogaol on DM-associated periodontitis is not well known. In this study, the effects of 6-shogaol on AGEs-induced oxidative and anti-oxidative responses, and IL-6 and ICAM-1 expression in human gingival fibroblasts (HGFs) were investigated. When HGFs were cultured with 6-shogaol and AGEs, the activities of reactive oxygen species (ROS) and antioxidant enzymes (heme oxygenase-1 [HO-1] and NAD(P)H quinone dehydrogenase 1 [NQO1]), and IL-6 and ICAM-1 expressions were investigated. RAGE expression and phosphorylation of MAPKs and NF-κB were examined by western blotting. 6-Shogaol significantly inhibited AGEs-induced ROS activity, and increased HO-1 and NQO1 levels compared with the AGEs-treated cells. The AGEs-stimulated expression levels of receptor of AGE (RAGE), IL-6 and ICAM-1 and the phosphorylation of p38, ERK and p65 were attenuated by 6-shogaol. These results suggested that 6-shogaol inhibits AGEs-induced inflammatory responses by regulating oxidative and anti-oxidative activities and may have protective effects on periodontitis with DM.
- (徳島大学機関リポジトリ)
- ● Metadata: 114673
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.3390/molecules24203705
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31619000
- ● Summary page in Scopus @ Elsevier: 2-s2.0-85073474436
(徳島大学機関リポジトリ: 114673, DOI: 10.3390/molecules24203705, PubMed: 31619000, Elsevier: Scopus) Eijiro Sakamoto, Jun-ichi Kido, Ryosuke Takagi, Yuji Inagaki, Koji Naruishi, Toshihiko Nagata and Hiromichi Yumoto :
Advanced glycation end-product 2 and Porphyromonas gingivalis lipopolysaccharide increase sclerostin expression in mouse osteocyte-like cells,
Bone, Vol.122, 22-30, 2019.- (要約)
- Sclerostin is a secreted glycoprotein that is mainly expressed in osteocytes, exerts negative effects on bone formation, and is present at elevated levels in diabetes mellitus (DM). Periodontitis is an infectious disease caused by periodontopathic bacteria, a complication of DM, and sometimes associated with severe inflammation and alveolar bone resorption. Advanced glycation end-products (AGEs) are a major pathogen in DM complications and adversely influence periodontitis in DM patients. In the present study, the effects of AGE2 and Porphyromonas gingivalis lipopolysaccharide (P-LPS) on the expression of sclerostin in mouse osteocyte-like cells (MLO-Y4-A2 cells) and its function in osteoblast differentiation were investigated. AGE2 and P-LPS up-regulated the expressions of receptor of AGE (RAGE) and Toll-like receptor 2 (TLR2), respectively, and significantly up-regulated that of sclerostin and interleukin 6 (IL-6) in osteocytes. Sclerostin, RAGE and TLR2 levels were synergistically increased by AGE2 and P-LPS. The siRNAs of RAGE and TLR2 significantly inhibited AGE2- and P-LPS-induced sclerostin expression. AGE2 up-regulated sclerostin expression in osteocyte-like cells via the RAGE, ERK and JNK, and NF-κB signal pathways. On the other hand, P-LPS elevated sclerostin levels via the TLR2, JNK and p38, and NF-κB signal pathways. When osteocytes pre-treated with AGE2 and P-LPS and osteoblastic cells (MC3T3-E1) were co-cultured in the medium with a sclerostin-neutralizing antibody, AGE2- and P-LPS-induced decreases in alkaline phosphatase activity and Runx2 expression in osteoblastic cells were significantly inhibited by the sclerostin-neutralizing antibody. These results suggest that AGE2 and P-LPS influence bone metabolism and inflammation through the regulation of sclerostin expression, and may aggravate periodontitis with DM.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1016/j.bone.2019.02.001
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30735798
- ● Search Scopus @ Elsevier (PMID): 30735798
- ● Search Scopus @ Elsevier (DOI): 10.1016/j.bone.2019.02.001
(DOI: 10.1016/j.bone.2019.02.001, PubMed: 30735798) Jung-Hwan Lew, Koji Naruishi, Yukari Kajiura, Yasufumi Nishikawa, Takahisa Ikuta, Jun-ichi Kido and Toshihiko Nagata :
High Glucose-Mediated Cytokine Regulation in Gingival Fibroblasts and THP-1 Macrophage: a Possible Mechanism of Severe Periodontitis with Diabetes.,
Cellular Physiology and Biochemistry, Vol.50, No.3, 973-986, 2018.- (要約)
- Diabetic conditions such as HG induce IL-1 and sIL-6R production from macrophages in inflammatory periodontal tissues and may exacerbate the periodontitis synergistically via MMP-1 production from HGFs.
- (徳島大学機関リポジトリ)
- ● Metadata: 113370
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1159/000494481
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30355945
- ● Search Scopus @ Elsevier (PMID): 30355945
- ● Search Scopus @ Elsevier (DOI): 10.1159/000494481
(徳島大学機関リポジトリ: 113370, DOI: 10.1159/000494481, PubMed: 30355945) Koji Naruishi :
Association between oral frailty and geriatric conditions,
OBM Geriatrics, Vol.2, No.4, 2018.- (出版サイトへのリンク)
- ● Publication site (DOI): 10.21926/obm.geriatr.1804016
- (文献検索サイトへのリンク)
- ● Search Scopus @ Elsevier (DOI): 10.21926/obm.geriatr.1804016
(DOI: 10.21926/obm.geriatr.1804016) Kohei Nonaka, Yukari Kajiura, Mika Bandou, Eijiro Sakamoto, Yuji Inagaki, JH Lew, Koji Naruishi, Takahisa Ikuta, Kaya Yoshida, Tesuo Kobayashi, Hiromasa Yoshie, Toshihiko Nagata and Jun-ichi Kido :
Advanced glycation end-products increase IL-6 and ICAM-1 expression via RAGE, MAPK and NF-kB pathways in human gingival fibroblasts,
Journal of Periodontal Research, Vol.53, No.3, 334-344, 2018.- (要約)
- Diabetes mellitus (DM) is a risk factor for periodontal diseases and may exacerbate the progression of the pathogenesis of periodontitis. Advanced glycation end-products (AGEs) cause DM complications relative to levels of glycemic control and larger amounts accumulate in the periodontal tissues of patients with periodontitis and DM. In the present study, we investigated the effects of AGEs on the expression of inflammation-related factors in human gingival fibroblasts (HGFs) to elucidate the impact of AGEs on DM-associated periodontitis. HGFs were cultured with or without AGEs. Cell viability was examined, and RNA and protein fractions were isolated from AGE-treated cells. The expression of interleukin (IL)-6, intercellular adhesion molecule-1 (ICAM-1), and the receptor for AGE (RAGE) was investigated using reverse transcription-polymerase chain reaction, quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay, and reactive oxygen species activity was measured using a kit with 2',7'-dichlorofluorescin diacetate. Human monocytic cells (THP-1) labeled with a fluorescent reagent were co-cultured with HGFs treated with AGEs and IL-6 siRNA, and the adhesive activity of THP-1 cells to HGFs was assessed. The expression of IL-6 and ICAM-1 was examined when HGFs were pretreated with recombinant human IL-6, the siRNAs of RAGE and IL-6, and inhibitors of MAPK and NF-κB, and then cultured with and without AGEs. The phosphorylation of MAPK and NF-κB was assessed using western blotting. AGEs increased the mRNA and protein expressions of RAGE, IL-6, ICAM-1 and reactive oxygen species activity in HGFs, and promoted the adhesion of THP-1 cells to HGFs, but had no effect on cell viability until 72 hours. Recombinant human IL-6 increased ICAM-1 expression in HGFs, while the siRNAs of RAGE and IL-6 inhibited AGE-induced IL6 and ICAM1 mRNA expression, and IL-6 siRNA depressed AGE-induced THP-1 cell adhesion. AGEs increased the phosphorylation of p38 and ERK MAPKs, p65 NF-κB and IκBα, while inhibitors of p38, ERK MAPKs and NF-κB significantly decreased AGE-induced IL-6 and ICAM-1 expression. AGEs increase IL-6 and ICAM-1 expression via the RAGE, MAPK and NF-κB pathways in HGFs and may exacerbate the progression of the pathogenesis of periodontal diseases.
- (キーワード)
- Antigens, Neoplasm / Diabetes Complications / Fibroblasts / Gingiva / Glycation End Products, Advanced / Humans / Intercellular Adhesion Molecule-1 / Interleukin-6 / MAP Kinase Signaling System / Mitogen-Activated Protein Kinase Kinases / Mitogen-Activated Protein Kinases / NF-kappa B / Periodontitis / Phosphorylation / Reactive Oxygen Species / THP-1 Cells
- (徳島大学機関リポジトリ)
- ● Metadata: 113617
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1111/jre.12518
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29193068
- ● Summary page in Scopus @ Elsevier: 2-s2.0-85036593558
(徳島大学機関リポジトリ: 113617, DOI: 10.1111/jre.12518, PubMed: 29193068, Elsevier: Scopus) Koji Naruishi, Hiromichi Yumoto and Jun-ichi Kido :
Clinical effects of low body mass index on geriatric status in elderly patients.,
Experimental Gerontology, Vol.110, 86-91, 2018.- (要約)
- ). Significant associations of low BMI to several geriatric factors such as loss of posterior occlusion, cognitive impairment were observed in both male and female. FIM scores in above cut-off point group were significantly higher than in below cut-off point group in female (FIM gain, P = 0.0005; FIM efficiency, P = 0.0025, Mann-Whitney U test). On the other hand, there were no significant differences between low and above BMI cut-off point in FIM scores of male patients.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1016/j.exger.2018.05.017
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29842897
- ● Search Scopus @ Elsevier (PMID): 29842897
- ● Search Scopus @ Elsevier (DOI): 10.1016/j.exger.2018.05.017
(DOI: 10.1016/j.exger.2018.05.017, PubMed: 29842897) Koji Naruishi, Yasufumi Nishikawa, Jun-ichi Kido, Akihiro Fukunaga and Toshihiko Nagata :
Relationship of aspiration pneumonia to cognitive impairment and oral condition: a cross-sectional study.,
Clinical Oral Investigations, Vol.22, No.7, 2575-2580, 2018.- (要約)
- Early and simple evaluation of the oral condition and cognitive function can predict the risk of aspiration pneumonia.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1007/s00784-018-2356-7
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29388021
- ● Summary page in Scopus @ Elsevier: 2-s2.0-85045039612
(DOI: 10.1007/s00784-018-2356-7, PubMed: 29388021, Elsevier: Scopus) Yukari Kajiura, Yasufumi Nishikawa, Hwan Jung Lew, Jun-ichi Kido, Toshihiko Nagata and Koji Naruishi :
b-carotene suppresses Porphyromonas gingivalis lipopolysaccharide-mediated cytokine production in THP-1 monocytes cultured with high glucose condition.,
Cell Biology International, Vol.42, No.1, 105-111, 2018.- (要約)
- Periodontitis is associated with development of diabetes mellitus. Although lipopolysaccharide (LPS) of Porphyromonas gingivalis (Pg), a major pathogen of periodontitis, may lead the progression of diabetes complications, the precise mechanisms are unclear. We, therefore, investigated the effects of β-carotene on production of Pg LPS-induced inflammatory cytokines in human monocytes cultured high glucose (HG) condition. THP-1 cells were cultured under 5.5 mM or 25 mM glucose conditions, and cells were stimulated with Pg LPS. To investigate the productivity of TNF-α, IL-6, and MCP-1, cell supernatants were collected for ELISA. To examine the effects of NF-kB signals on cytokine production, Bay11-7082 was used. HG enhanced Pg LPS-induced production of TNF-α, IL-6, and MCP-1 via NF-kB signals in THP-1. β-carotene suppressed the enhancement of the Pg LPS-induced cytokine production in THP-1 via NF-κB inactivation. Our results suggest that β-carotene might be a potential anti-inflammatory nutrient for circulating Pg LPS-mediated cytokine production in diabetic patients with periodontitis.
- (徳島大学機関リポジトリ)
- ● Metadata: 112503
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1002/cbin.10873
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28906038
- ● Search Scopus @ Elsevier (PMID): 28906038
- ● Search Scopus @ Elsevier (DOI): 10.1002/cbin.10873
(徳島大学機関リポジトリ: 112503, DOI: 10.1002/cbin.10873, PubMed: 28906038) Koji Naruishi and Yasufumi Nishikawa :
Swallowing impairment is a significant factor for predicting life prognosis of elderly at the end of life.,
Aging Clinical and Experimental Research, Vol.30, No.1, 77-80, 2018.- (要約)
- A total of 320 elderly patients was enrolled (male/female 151/169; averaged age: male 84.7 ± 5.9 year, female 86.8 ± 6.3 year) and retrospective analyses were performed. The elderly patients were classified as either: (1) with or without past illness of aspiration pneumonia; (2) with or without incidence of cerebrovascular disorder; (3) impaired or normal cognitive function; (4) impaired or normal swallowing function, and performed Kaplan-Meier survival analysis. Swallowing function was examined using video endoscopic (VE) evaluation method. The Kaplan-Meier analysis of the number of days from implementation of VE test (day 0) to death was evaluated with the log-rank Mantel-Cox test. The maximum follow-up time recorded was 180 days.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1007/s40520-017-0756-1
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28391586
- ● Search Scopus @ Elsevier (PMID): 28391586
- ● Search Scopus @ Elsevier (DOI): 10.1007/s40520-017-0756-1
(DOI: 10.1007/s40520-017-0756-1, PubMed: 28391586) Chie Wada -Mihara, Hiroyuki Seto, Hirofumi Ohba, Kaku Tokunaga, Jun-ichi Kido, Toshihiko Nagata and Koji Naruishi :
Local administration of calcitonin inhibits alveolar bone loss in an experimental periodontitis in rats.,
Biomedicine & Pharmacotherapy, Vol.97, No.1, 765-770, 2018.- (要約)
- Calcitonin (CTN), a calcium regulatory hormone, promotes calcium diuresis from the kidney and suppresses bone resorption. The objective of this study was to evaluate whether the topical and intermittent application of CTN inhibits alveolar bone resorption using ligature-induced experimental periodontitis in rats. Experimental periodontitis was induced by placing a nylon ligature around maxillary molars of 8-week-old male Wistar rats for 20 days. Thirty-two rats were divided into four groups: basal sham control group, periodontitis group, periodontitis plus 0.2 U CTN (low dose), and periodontitis plus 1.0 U CTN (high dose) group. To investigate the effects of CTN on alveolar bone resorption, CTN was topically injected into the palatal gingivae every 2 days after ligature removal (day 0). Micro-computed tomography (CT) analysis was performed for linear parameter assessment of alveolar bone on day 5 and day 14. Periodontal tissues were examined histo-pathologically to assess the differences among the study groups. Micro-CT images showed that alveolar bone resorption was induced statistically around the molar of ligatured rats on day 5 and day 14. The amount of bone resorption was more severe on day 14 than that on day 5. On day 5, only high-dose CTN treatment significantly suppressed bone resorption. In addition, both doses of CTN significantly suppressed bone resorption on day 14. Histological examination clarified that there were fewer TRAP-positive cells in the CTN treatment groups than in the periodontitis group on day 5. Local administration of CTN decreased alveolar bone resorption by regulating osteoclast activation in rats with periodontitis.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1016/j.biopha.2017.10.165
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29107933
- ● Search Scopus @ Elsevier (PMID): 29107933
- ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2017.10.165
(DOI: 10.1016/j.biopha.2017.10.165, PubMed: 29107933) Yuka Hiroshima, Eijiro Sakamoto, Kaya Yoshida, Kaori Abe, Koji Naruishi, Takenori Yamamoto, Yasuo Shinohara, Jun-ichi Kido and Carolyn L Geczy :
Advanced glycation end-products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells.,
Journal of Cellular Biochemistry, Vol.119, No.2, 1591-1603, 2018.- (要約)
- Accumulation of advanced glycation end-products (AGEs) in periodontal tissues of patients with diabetes mellitus aggravates periodontitis, but the mechanisms are unknown. Calprotectin, a heterocomplex of S100A8 and S100A9 proteins, is a constitutive cytoplasmic component of healthy gingival epithelial cells. This study aimed at investigating the effects of AGE and Porphyromonas gingivalis lipopolysaccharide (PgLPS) on calprotectin expression in the human gingival epithelial cell line OBA-9. AGE and PgLPS increased the expression of S100A8 and S100A9 mRNAs, and AGE + PgLPS co-stimulation amplified their expression in OBA-9 cells. A higher concentration of calprotectin in cell lysates was also induced by stimulation with AGE and/or PgLPS. S100A8 was mainly translocated from the nucleus to the cytoplasm by AGE stimulation, while cytoplasmic localization of S100A9 was not altered following stimulation with AGE and/or PgLPS. Calprotectin was found in the cytoplasm of BSA-treated cells, but cytoplasmic and nuclear localization was observed following stimulation with AGE and/or PgLPS. AGE-induced S100A8, and S100A9 mRNA expression was partially suppressed by RAGE-specific siRNA. In contrast, PgLPS-induced S100A8 and S100A9 mRNA expression was strongly suppressed by TLR2-specific siRNA. Furthermore, the inhibition of p38, JNK MAPK, and NF-κB attenuated AGE- and PgLPS-induced S100A8 and S100A9 mRNA expression. Taken together, these results demonstrate that AGE acts in synergy with PgLPS to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF-κB signaling pathways, resulting in increased activation of calprotectin (S100A8/S100A9) in human gingival epithelial cells. Our results suggest that calprotectin may be involved in the pathogenesis of diabetic periodontitis. This article is protected by copyright. All rights reserved.
- (徳島大学機関リポジトリ)
- ● Metadata: 119200
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1002/jcb.26319
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28771806
- ● Search Scopus @ Elsevier (PMID): 28771806
- ● Search Scopus @ Elsevier (DOI): 10.1002/jcb.26319
(徳島大学機関リポジトリ: 119200, DOI: 10.1002/jcb.26319, PubMed: 28771806) Jun-ichi Kido, Shinya Murakami, Masahiro Kitamura, Manabu Yanagita, Koichi Tabeta, Kazuhisa Yamazaki, Hiromasa Yoshie, Hisashi Watanabe, Yuichi Izumi, Reiko Suda, Matsuo Yamamoto, Hideki Shiba, Tsuyoshi Fujita, Hidemi Kurihara, Mitsuharu Mizuno, Akihiro Mishima, Nobumasa Kawahara, Kazuhiro Hashimoto, Koji Naruishi and Toshihiko Nagata :
Useful Immunochromatographic Assay of Calprotectin in Gingival Crevicular Fluid for Diagnosis of Diseased Sites in Patients with Periodontal Diseases.,
Journal of Periodontology, 1-19, 2017.- (要約)
- Determination of GCF calprotectin using a novel IC chip system is useful for diagnosis of periodontal diseases.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1902/jop.2017.170206
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28875823
- ● Search Scopus @ Elsevier (PMID): 28875823
- ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2017.170206
(DOI: 10.1902/jop.2017.170206, PubMed: 28875823) Koji Naruishi :
Association between Oral Conditions and Returning Home after Discharge in Elderly Patients,
Geriatrics, Vol.2, No.3, 28, 2017.- (徳島大学機関リポジトリ)
- ● Metadata: 115109
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.3390/geriatrics2030028
- (文献検索サイトへのリンク)
- ● Search Scopus @ Elsevier (DOI): 10.3390/geriatrics2030028
(徳島大学機関リポジトリ: 115109, DOI: 10.3390/geriatrics2030028) Yukari Kajiura, Hwan Jung Lew, Takahisa Ikuta, Yasufumi Nishikawa, Jun-ichi Kido, Toshihiko Nagata and Koji Naruishi :
Clinical Significance of GCF sIL-6R and Calprotectin to Evaluate the Periodontal Inflammation.,
Annals of Clinical Biochemistry, Vol.54, No.6, 664-670, 2017.- (要約)
- Both GCF sIL-6R and calprotectin levels are significant bio-markers to evaluate the periodontal inflammation.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1177/0004563216680232
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27810997
- ● Search Scopus @ Elsevier (PMID): 27810997
- ● Search Scopus @ Elsevier (DOI): 10.1177/0004563216680232
(DOI: 10.1177/0004563216680232, PubMed: 27810997) 美原(和田) 智恵, 成石 浩司, 板東 美香, 西川 泰史, Lew Jung-Hwan, 坂本 英次郎, 生田 貴久, 河野 薫, 梶浦 由加里, 橋本 万里, 中島 由紀子, 稲垣 裕司, 二宮 雅美, 木戸 淳一, 永田 俊彦 :
Post clinical clerkship-OSCEを見据えた歯周病科での模擬OSCEの概要,
Journal of Oral Health and Biosciences, Vol.29, No.2, 49-53, 2017年.- (徳島大学機関リポジトリ)
- ● Metadata: 111059
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.20738/johb.29.2_49
- (文献検索サイトへのリンク)
- ● Search Scopus @ Elsevier (DOI): 10.20738/johb.29.2_49
(徳島大学機関リポジトリ: 111059, DOI: 10.20738/johb.29.2_49) Yasufumi Nishikawa, Yukari Kajiura, Hwan Jung Lew, Jun-ichi Kido, Toshihiko Nagata and Koji Naruishi :
Calprotectin Induces IL-6 and MCP-1 Production via Toll-Like Receptor 4 Signaling in Human Gingival Fibroblasts.,
Journal of Cellular Physiology, Vol.232, No.7, 1862-1871, 2017.- (要約)
- Calprotectin, a heterodimer of S100A8 and S100A9 molecules, is associated with inflammatory diseases such as inflammatory bowel disease. We have reported that calprotectin levels in gingival crevicular fluids of periodontitis patients are significantly higher than in healthy subjects. However, the functions of calprotectin in pathophysiology of periodontitis are still unknown. The aim of this study is to investigate the effects of calprotectin on the productivity of inflammatory cytokines in human gingival fibroblasts (HGFs). The HGFs cell line CRL-2014® (ATCC) were cultured, and total RNAs were collected to examine the expression of TLR2/4 and RAGE mRNA using RT-PCR. After the cells were treated with S100A8, S100A9, and calprotectin, supernatants were collected and the levels of IL-6 and MCP-1 were measured using ELISA methods. To examine the intracellular signals involved in calprotectin-induced cytokine production, several chemical inhibitors were used. Furthermore, after the siRNA-mediated TLR4 down-regulated cells were treated with S100A8, S100A9, and calprotectin, the levels of IL-6 and MCP-1 were also measured. HGFs showed greater expression of TLR4 mRNA, but not TLR2 and RAGE mRNA compared with human oral epithelial cells. Calprotectin increased significantly the production of MCP-1 and IL-6 in HGFs, and the cytokine productions were significantly suppressed in the cells treated with MAPKs, NF-B, and TLR4 inhibitors. Furthermore, calprotectin-mediated MCP-1 and IL-6 production were significantly suppressed in TLR4 down-regulated cells. Taken together, calprotectin induces IL-6 and MCP-1 production in HGFs via TLR4 signaling that involves MAPK and NF-B, resulting in the progression of periodontitis. J. Cell. Physiol. 232: 1862-1871, 2017. © 2016 Wiley Periodicals, Inc.
- (キーワード)
- Antigens, Neoplasm / Cell Line, Tumor / 細胞増殖·分化 (cell proliferation and differentiation) / Chemokine CCL2 / Down-Regulation / Fibroblasts / Gene Expression Regulation / Gingiva / Humans / Inflammation Mediators / Interleukin-6 / Intracellular Space / Leukocyte L1 Antigen Complex / Mitogen-Activated Protein Kinases / Models, Biological / NF-kappa B / Protein Kinase Inhibitors / RNA, Messenger / RNA, Small Interfering / 炎症性サイトカイン受容体の情報伝達 (Signal transduction of proinflammatory cytokine receptors) / Sulfonamides / Toll-Like Receptor 4 / Transfection
- (徳島大学機関リポジトリ)
- ● Metadata: 111725
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1002/jcp.25724
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27925202
- ● Summary page in Scopus @ Elsevier: 2-s2.0-85008440585
(徳島大学機関リポジトリ: 111725, DOI: 10.1002/jcp.25724, PubMed: 27925202, Elsevier: Scopus) Koji Naruishi, Keiji Oishi, Yuuji Inagaki, Masumi Horibe, Mika Bandou, Masami Ninomiya, K Kawahara, J Minakuchi, S Kawashima, K Shima, Jun-ichi Kido and Toshihiko Nagata :
Association between Periodontal Condition and Kidney Dysfunction in Japanese Adults: A Cross-Sectional Study,
Clinical and Experimental Dental Research, Vol.2, No.2, 1-8, 2016.- (徳島大学機関リポジトリ)
- ● Metadata: 115061
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1002/cre2.39
- (文献検索サイトへのリンク)
- ● Search Scopus @ Elsevier (DOI): 10.1002/cre2.39
(徳島大学機関リポジトリ: 115061, DOI: 10.1002/cre2.39) K Takeuchi-Hatanaka, T Yasuda, Koji Naruishi, K Katsuragi-Fuke, J Inubushi, H Ootsuki, H Maeda and S Takashiba :
Effects of new over-the-counter periodontal ointment-containing applicator with single-tuft brush on cytokine levels in gingival crevicular fluid during supportive periodontal therapy phase: a randomized double-blind clinical trial.,
Journal of Periodontal Research, Vol.51, No.3, 321-331, 2016.- (要約)
- The levels of IL-1β, IL-6, IL-8 and TNF-α remained significantly lower in the test group compared to the placebo group. In the placebo group, when the probing pocket depth at baseline was 4 mm, IL-1β increased, particularly in the second molar tooth, and the greatest increase was seen when PPD at baseline was 5-6 mm. In the test group, IL-1β decreased markedly in cases with furcation involvement and low bleeding on probing at baseline. In both groups, IL-1β, IL-6 and TNF-α were closely correlated with each other.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1111/jre.12311
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26251312
- ● Summary page in Scopus @ Elsevier: 2-s2.0-84938650739
(DOI: 10.1111/jre.12311, PubMed: 26251312, Elsevier: Scopus) 成石 浩司, 梶浦 由加里, 西川 泰史, 板東 美香, 木戸 淳一, 永田 俊彦 :
培養歯肉線維芽細胞におけるクリプトタンシノンによる炎症関連分子の産生抑制効果,
日本歯科保存学雑誌, Vol.58, No.3, 212-218, 2015年.- (要約)
- 目的 : 漢方薬 (生薬) タンジンの主成分であるクリプトタンシノンは, 抗がん作用や抗炎症作用をもつことが知られている. しかしながら, クリプトタンシノンが歯周組織の炎症に対してどのような影響を及ぼすのかは不明である. 本研究の目的は, 歯肉線維芽細胞を標的として, その炎症関連分子の産生に及ぼすクリプトタンシノンの影響を調べることである. 方法 : 細胞は歯肉線維芽細胞CRL-2014TM (ATCC) を用いた. クリプトタンシノンの濃度依存的な細胞障害作用の有無は, トリパンブルー染色法を用いて各濃度間における生細胞率の差を比較検討して評価した. 歯肉線維芽細胞のサイトカイン産生は, 市販のELISAキットを用いて, インターロイキン (IL) -1βで細胞を24時間刺激した後のIL-6およびVEGF産生量を測定して検討した. 一方, タンパク質分解酵素カテプシンLの産生は, IL-1βで細胞を24時間刺激した後に回収した全細胞タンパク質を用いて, ウエスタンブロット法によって検討した. なお, クリプトタンシノンはIL-1β添加の1時間前に細胞培養系に添加した. 各群における差異は, ANOVA Tukey-KramerのHSD検定によって有意差を検討した. 結果 : クリプトタンシノンは, 10μmol/lまでは歯肉線維芽細胞の生細胞率に影響は与えないが, 100μmol/lでは有意に生細胞率を低下させた. また, 歯肉線維芽細胞におけるIL-1β誘導性のIL-6産生およびカテプシンL産生は, 10μmol/lクリプトタンシノンの添加によって著明に減少した. 一方, IL-1β誘導性のVEGF産生は, クリプトタンシノンの添加によっても変化しなかった. 結論 : クリプトタンシノンは, 歯肉線維芽細胞におけるIL-1β誘導性IL-6およびカテプシンLの産生を抑制することで, 歯周組織の炎症を抑制する可能性が示唆された.
- (キーワード)
- クリプトタンシノン / 歯肉線維芽細胞 / 歯周炎症 / IL-1β / periodontal inflammation
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.11471/shikahozon.58.212
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390001205520665472
- ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.58.212
(DOI: 10.11471/shikahozon.58.212, CiNii: 1390001205520665472) Jun-ichi Kido, Yukiko Bandou, Mika Bandou, Yukari Kajiura, Yuka Hiroshima, Yuji Inagaki, Hiromi Murata, Takahisa Ikuta, Reiko Kido, Koji Naruishi, Makoto Funaki and Toshihiko Nagata :
YKL-40 level in gingival crevicular fluid from patients with periodontitis and type 2 diabetes,
Oral Diseases, Vol.21, No.5, 667-673, 2015.- (要約)
- YKL-40 is a chitin-binding glycoprotein, the level of which increases in inflammatory diseases, diabetes mellitus (DM), cardiovascular diseases, and tumors. Gingival crevicular fluid (GCF) contains many proteins and markers of periodontitis. The purpose of this study was to investigate YKL-40 level in GCF from patients with periodontitis and DM and the association between YKL-40 level and chronic periodontitis (CP) or DM. The subjects were 121 patients with DM, CP, DM and periodontitis (DM-P), and healthy subjects (H). GCF was collected using paper strips after the sites for GCF collection were clinically evaluated for probing depth (PD), gingival index (GI), and bleeding on probing (BOP). YKL-40 in GCF was identified by Western blotting, and its level was determined by ELISA. YKL-40 was contained in GCF samples from H, DM, CP, and DM-P sites, and its levels (amount and concentration) in CP and DM-P were significantly higher than those in H and DM. GCF YKL-40 level significantly correlated with PD and GI, and its level in BOP-positive sites was significantly higher than that in BOP-negative ones. GCF YKL-40 level was elevated in periodontitis, but not DM. YKL-40 in GCF may be an inflammatory marker for periodontitis.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1111/odi.12334
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25740558
- ● Summary page in Scopus @ Elsevier: 2-s2.0-84930271794
(DOI: 10.1111/odi.12334, PubMed: 25740558, Elsevier: Scopus) 稲垣 裕司, 中島 由紀子, 堀部 ますみ, 生田 貴久, 梶浦 由加里, 成石 浩司, 木戸 淳一, 永田 俊彦 :
肥満糖尿病ラット歯周炎の歯肉組織におけるオステオポンチンの局在,
日本歯周病学会会誌, Vol.67, No.4, 149-158, 2015年.- (出版サイトへのリンク)
- ● Publication site (DOI): 10.2329/perio.57.149
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390001204416151552
- ● Search Scopus @ Elsevier (DOI): 10.2329/perio.57.149
(DOI: 10.2329/perio.57.149, CiNii: 1390001204416151552) Koji Naruishi, Akiko Kunita, Katsuyuki Kubo, Toshihiko Nagata, Shogo Takashiba and Seiji Adachi :
Predictors of improved functional outcome in elderly inpatients after rehabilitation: a retrospective study.,
Clinical Interventions in Aging, Vol.9, 2133-2141, 2014.- (要約)
- Age and disorder of oral function may be significant predictors of improved functional capacity after rehabilitation for elderly inpatients.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.2147/CIA.S73388
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25584025
- ● Search Scopus @ Elsevier (PMID): 25584025
- ● Search Scopus @ Elsevier (DOI): 10.2147/CIA.S73388
(DOI: 10.2147/CIA.S73388, PubMed: 25584025) Kazuhiro Omori, Yoshihisa Hanayama, Koji Naruishi, Kentaro Akiyama, Hiroshi Maeda, Fumio Otsuka and Shogo Takashiba :
Gingival overgrowth caused by vitamin C deficiency associated with metabolic syndrome and severe periodontal infection: a case report.,
Clinical Case Reports, Vol.2, No.6, 286-295, 2014.- (要約)
- It has been suggested that vitamin C deficiency/scurvy is associated with gingival inflammatory changes; however, the disorder is very infrequently encountered in the modern era. Here, we report a case of extensive gingival overgrowth caused by vitamin C deficiency associated with metabolic syndrome and severe periodontal infection.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1002/ccr3.114
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25548632
- ● Search Scopus @ Elsevier (PMID): 25548632
- ● Search Scopus @ Elsevier (DOI): 10.1002/ccr3.114
(DOI: 10.1002/ccr3.114, PubMed: 25548632) 久保 克行, 目黒 道夫, 竹内 いずみ, 中山 良子, 加藤 真由美, 成石 浩司, 澤田 弘一, 足立 誠司, 山下 裕 :
ADL,認知機能の低下及び低栄養を併発した老年症候群患者は摂食嚥下機能が低下する,
全国自治体病院協議会雑誌, Vol.53, No.6, 943-948, 2014年. Tetsuo Fujita, Takefumi Satoh, L Terry Timme, Takahiro Hirayama, X Julie Zhu, Nobuyuki Kusaka, Koji Naruishi, Guang Yang, Alexei Goltsov, Jianxiang Wang, T Maria Vlachaki, S Bin Teh, E Butler Brian and C Timothy Thompson :
Combined therapeutic effects of adenoviral vector-mediated GLIPR1 gene therapy and radiotherapy in prostate and bladder cancer models.,
Urologic Oncology: Seminars and Original Investigations, Vol.32, No.2, 92-100, 2014.- (要約)
- Combining AdGlipr1 (AdGLIPR1) with radiotherapy may achieve additive or synergistic tumor control in selected prostate and bladder tumors, and additional therapeutic effects may result with repeated treatment cycles.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1016/j.urolonc.2012.10.007
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23433894
- ● Search Scopus @ Elsevier (PMID): 23433894
- ● Search Scopus @ Elsevier (DOI): 10.1016/j.urolonc.2012.10.007
(DOI: 10.1016/j.urolonc.2012.10.007, PubMed: 23433894) Naoki Takizawa, Shunsuke Sawada, Naoyuki Chosa, Akira Ishisaki and Koji Naruishi :
Secreted caveolin-1 enhances periodontal inflammation by targeting gingival fibroblasts.,
Biomedical Research, Vol.34, No.1, 1-11, 2013.- (要約)
- Caveolin-1 (Cav-1) is a membrane protein. Recently, it has been reported that secreted Cav-1 induces angiogenesis in inflammatory microenvironment. However, it is unclear that Cav-1 regulates gingival inflammation. Therefore, we investigated the Cav-1 function to periodontal cells. Expression of Cav-1 in human periodontitis tissues was examined pathologically. Secretion of Cav-1 from human gingival fibroblasts (HGFs) or human periodontal ligament cells (HPLFs) treated with IL-1 and TNF- was examined using Western blotting. Likewise, intracellular signals induced by Cav-1 were examined. Finally, we examined whether the secreted Cav-1 induces production of inflammatory mediators in HGFs using ELISA or qRT-PCR. Pathologically, high expression of Cav-1 was observed in human periodontitis tissues. Cav-1 secretion increased in both cultured HGFs and HPLFs treated with IL-1 and TNF-. Cav-1 induced phosphorylation of JNK and ERK, but not Stat3 in HGFs. Furthermore, Cav-1 increased proMMP-1 and VEGF secretion in HGFs, and the VEGF secretion was statistically suppressed by JNK inhibitor SP600125, but not ERK inhibitor PD98059. ProMMP-1 secretion was suppressed statistically by both SP600125 and PD98059. In addition, Cav-1 increased significantly MMP-1, -10 and -14 mRNA expressions, whereas no increase of TIMPs mRNA was observed in HGFs treated with Cav-1. These data suggest that secreted Cav-1 derived from periodontal fibroblastic cells enhances inflammation-related several proteases and VEGF secretion in HGFs via MAPKs pathway, resulting in progression of periodontitis through induction of tissue degradation or angiogenesis.
- (キーワード)
- Anthracenes / Blotting, Western / Caveolin 1 / Cell Survival / Cells, Cultured / Extracellular Signal-Regulated MAP Kinases / Fibroblasts / フラボノイド (flavonoids) / Gingiva / Humans / 炎症 (inflammation) / Interleukin-1beta / JNK Mitogen-Activated Protein Kinases / Matrix Metalloproteinase 1 / Matrix Metalloproteinase 10 / Matrix Metalloproteinase 14 / Periodontal Ligament / 歯周病 (periodontitis) / 酸化的リン酸化 (oxidative phosphorylation) / RNA, Messenger / STAT3 Transcription Factor / シグナル伝達 (signal transduction) / Tumor Necrosis Factor-alpha / Up-Regulation / 血管内皮増殖因子 (vascular endothelial growth factor)
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.2220/biomedres.34.1
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23428975
- ● Summary page in Scopus @ Elsevier: 2-s2.0-84874304488
(DOI: 10.2220/biomedres.34.1, PubMed: 23428975, Elsevier: Scopus) Shunsuke Sawada, Naoyuki Chosa, Akira Ishisaki and Koji Naruishi :
Enhancement of gingival inflammation induced by synergism of IL-1 and IL-6.,
Biomedical Research, Vol.34, No.1, 31-40, 2013.- (要約)
- Internleukin-1 (IL-1) and IL-6 are the most potent proinflammatory cytokines being involved in inflammatory diseases such as periodontitis. The objective of this study was to examine the synergistic effects of IL-1 and IL-6 on gingival inflammation by targeting cultured human gingival fibroblasts (HGFs). HGFs were treated with IL-1 or IL-6/soluble IL-6R (sIL-6R), and total RNA and total cell lysate were collected to examine expression of gp130 known as a signal transducer of IL-6 using qRT-PCR and Western blotting. IL-1-mediated IL-6 productivity in HGFs was examined using ELISA method. Likewise, after HGFs and THP-1 macrophages were treated with IL-1, TNF- and IL-6, sIL-6R productivity was examined. Next, HGFs were treated with IL-6/ sIL-6R after pretreatment of IL-1, and the intracellular signals were examined using Western blotting. Finally, various mRNA/protein expressions in HGFs treated with IL-6/sIL-6R after pretreatment of IL-1 were examined using qRT-PCR and ELISA method. IL-1 increased significantly both gp130 and IL-6 expression in HGFs. IL-6 increased significantly sIL-6R production in THP-1 macrophages but not HGFs. Co-stimulation with IL-1 and IL-6/sIL-6R induced dramatically the phosphorylation of Stat3, ERK and JNK in HGFs. Interestingly, expression of various inflammation- related molecules such as MMP-1, MCP-1, IL-1ra, bFGF and VEGF were enhanced by co-stimulation with IL-1 and IL-6/sIL-6R in HGFs. Gingival inflammation is regulated by HGFs affected by both IL-1 and IL-6/sIL-6R synergistically through induction of gp130 expression, resulting in progression of periodontitis.
- (キーワード)
- Blotting, Western / 細胞増殖·分化 (cell proliferation and differentiation) / Cells, Cultured / Chemokine CCL2 / Cytokine Receptor gp130 / Drug Synergism / Fibroblasts / Gene Expression Regulation / Gingiva / Humans / 炎症 (inflammation) / Interleukin 1 Receptor Antagonist Protein / Interleukin-1beta / Interleukin-6 / JNK Mitogen-Activated Protein Kinases / Matrix Metalloproteinase 1 / 歯周病 (periodontitis) / Phosphorylation / RNA, Messenger / STAT3 Transcription Factor / シグナル伝達 (signal transduction) / Tumor Necrosis Factor-alpha / 血管内皮増殖因子 (vascular endothelial growth factor)
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.2220/biomedres.34.31
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23428978
- ● Summary page in Scopus @ Elsevier: 2-s2.0-84874312974
(DOI: 10.2220/biomedres.34.31, PubMed: 23428978, Elsevier: Scopus) C Kudo, Koji Naruishi, H Maeda, Y Abiko, T Hino, M Iwata, C Mitsuhashi, S Murakami, T Nagasawa, Toshihiko Nagata, Satoshi Yoneda, Y Nomura, T Noguchi, Y Numabe, Y Ogata, T Sato, H Shimauchi, K Yamazaki, A Yoshimura and S Takashiba :
Assessment of the plasma/serum IgG test to screen for periodontitis.,
Journal of Dental Research, Vol.91, No.12, 1190-1195, 2012.- (要約)
- Chronic periodontitis is a silent infectious disease prevalent worldwide and affects lifestyle-related diseases. Therefore, efficient screening of patients is essential for general health. This study was performed to evaluate prospectively the diagnostic utility of a blood IgG antibody titer test against periodontal pathogens. Oral examination was performed, and IgG titers against periodontal pathogens were measured by ELISA in 1,387 individuals. The cut-off value of the IgG titer was determined in receiver operating characteristic curve analysis, and changes in periodontal clinical parameters and IgG titers by periodontal treatment were evaluated. The relationships between IgG titers and severity of periodontitis were analyzed. The best cut-off value of IgG titer against Porphyromonas gingivalis for screening periodontitis was 1.682. Both clinical parameters and IgG titers decreased significantly under periodontal treatment. IgG titers of periodontitis patients were significantly higher than those of healthy controls, especially in those with sites of probing pocket depth over 4 mm. Multiplied cut-off values were useful to select patients with severe periodontitis. A blood IgG antibody titer test for Porphyromonas gingivalis is useful to screen hitherto chronic periodontitis patients.
- (キーワード)
- Actinobacillus actinomycetemcomitans / Adult / Antibodies, Bacterial / Case-Control Studies / Chronic Periodontitis / Eikenella corrodens / Female / Humans / Immunoglobulin G / Male / Mass Screening / Middle Aged / Porphyromonas gingivalis / Prevotella intermedia / Prospective Studies / ROC Curve / Reference Values / Reproducibility of Results / Sensitivity and Specificity
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1177/0022034512461796
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23018816
- ● Search Scopus @ Elsevier (PMID): 23018816
- ● Search Scopus @ Elsevier (DOI): 10.1177/0022034512461796
(DOI: 10.1177/0022034512461796, PubMed: 23018816) Tamaki Takahashi, Shigeo Muro, Naoya Tanabe, Kunihiko Terada, Hirofumi Kiyokawa, Susumu Sato, Yuma Hoshino, Emiko Ogawa, Kazuko Uno, Koji Naruishi, Shogo Takashiba and Michiaki Mishima :
Relationship between periodontitis-related antibody and frequent exacerbations in chronic obstructive pulmonary disease.,
PLoS ONE, Vol.7, No.7, e40570, 2012.- (要約)
- The numbers of exacerbations and the rate of individuals with frequent exacerbations (at least two per year) were significantly lower in patients with higher IgG titer than those with normal IgG titer (0.8 vs. 1.2 per year, p= 0.045 and 14.3 vs. 38.6%, p= 0.009, respectively). Multivariate logistic regression analysis showed that being normal-IgG titer for periodontitis-related antibody significantly increased the risk of frequent exacerbations (relative risk, 5.27, 95% confidence interval, 1.30-25.7; p = 0.019) after adjusting for other possible confounders, such as a history of exacerbations in the past year, disease severity, COPD medication and smoking status.
- (キーワード)
- Aged / Aged, 80 and over / Antibodies, Bacterial / Cohort Studies / 細胞質分裂 (cytokinesis) / Disease Progression / Humans / Immunoglobulin G / Inflammation Mediators / Logistic Models / Male / Middle Aged / 歯周病 (periodontitis) / Porphyromonas gingivalis / Prognosis / Prospective Studies / Pulmonary Disease, Chronic Obstructive / Risk Factors
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1371/journal.pone.0040570
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22792372
- ● Search Scopus @ Elsevier (PMID): 22792372
- ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0040570
(DOI: 10.1371/journal.pone.0040570, PubMed: 22792372) Shinya Tsuge, Yasuyoshi Mizutani, Kazuhiro Matsuoka, Tatsuya Sawasaki, Yaeta Endo, Koji Naruishi, Hiroshi Maeda, Shogo Takashiba, Kazuya Shiogama, Ken-Ichi Inada and Yutaka Tsutsumi :
Specific in situ visualization of plasma cells producing antibodies against Porphyromonas gingivalis in gingival radicular cyst: application of the enzyme-labeled antigen method.,
The Journal of Histochemistry and Cytochemistry, Vol.59, No.7, 673-689, 2011.- (要約)
- The enzyme-labeled antigen method was applied to visualize plasma cells producing antibodies to Porphyromonas gingivalis, flora of the human oral cavity. Antibodies to P. gingivalis have reportedly been detected in sera of patients with periodontitis. Biotinylated bacterial antigens, Ag53, and four gingipain domains (Arg-pro, Arg-hgp, Lys-pro, and Lys-hgp) were prepared by the cell-free protein synthesis system using the wheat germ extract. In paraformaldehyde-fixed frozen sections of rat lymph nodes experimentally immunized with Ag53-positive and Ag53-negative P. gingivalis, plasma cells were labeled with biotinylated Arg-hgp and Lys-hgp. Antibodies to Ag53 were detected only in the nodes immunized with Ag53-positive bacteria. In two of eight lesions of gingival radicular cyst with inflammatory infiltration, CD138-positive plasma cells in frozen sections were signalized for Arg-hgp and Lys-hgp. An absorption study using unlabeled antigens confirmed the specificity of staining. The AlphaScreen method identified the same-type antibodies in tissue extracts but not in sera. Antibodies to Ag53, Arg-pro, and Lys-pro were undetectable. In two cases, serum antibodies to Arg-hgp and Lys-hgp were AlphaScreen positive, whereas plasma cells were scarcely observed within the lesions. These findings indicate the validity of the enzyme-labeled antigen method. This is the very first application of this novel histochemical technique to human clinical samples.
- (キーワード)
- Adult / Animals / Antibodies, Bacterial / Antigens, Bacterial / Bacterial Proteins / Biotinylation / Endopeptidase K / Female / Genes, Bacterial / Humans / Immunization / Lymph Nodes / Male / Middle Aged / Plasma Cells / Porphyromonas gingivalis / Radicular Cyst / Rats / Rats, Sprague-Dawley / Sensitivity and Specificity
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1369/0022155411408906
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21525188
- ● Search Scopus @ Elsevier (PMID): 21525188
- ● Search Scopus @ Elsevier (DOI): 10.1369/0022155411408906
(DOI: 10.1369/0022155411408906, PubMed: 21525188) Koji Naruishi, K Omori, H Maeda, N Sonoi, K Funakoshi, K Hirai, M Ishii, K Kubo, H Kobayashi, T Tomiyama, D Yamamoto, I Tanimoto, K Kunimatsu and S Takashiba :
Immune responses to porphyromonas gingivalis infection suppress systemic inflammatory response in experimental murine model.,
Journal of Biological Regulators and Homeostatic Agents, Vol.25, No.2, 195-202, 2011.- (要約)
- Periodontitis is a localized infectious disease caused by periodontopathic bacteria such as Porphyromonas gingivalis (P. gingivalis), and the severity correlates to significance of immune responses. Recently, it has been reported that periodontitis is associated with the development of systemic disease such as diabetes and atherosclerosis because of increasing invasion of oral pathogens to the circulation. However, the association between local and systemic infectious responses is still unclear. In the present study, we examined the differences of biological responses in animals with or without bacterial infection. After Balb/c mice were infected subcutaneously with live P. gingivalis W83, serum, skin and liver were collected according to experimental protocol. The skin and liver tissues were observed pathologically by haematoxylin-eosin staining, and serum IL-6 levels were measured using ELISA method. Throughout the experimental period, conditions of the mice were observed continuously. As expected, severe infiltration of leukocytes were observed at inflamed skin corresponding to the number of bacterial challenges. Although no inflammatory appearance of skin was observed, serum IL-6 levels were increased dramatically (P <0.01, Student's t-test) and liver tissues were injured in the mice without bacterial challenge. Interestingly, although severe inflammatory appearance of the skin was observed, serum IL-6 levels were not increased and no inflammatory responses were observed in the liver of the 3-times bacterially challenged group. Importantly, immunoglobulin G against P. gingivalis W83 was detected in the blood of mice with 3-times bacterial challenge corresponding to improvement of weight loss and survival. In conclusion, although multiple infections develop severe localized inflammation, the immune system should be sufficient to protect the systemic inflammatory responses.
- (キーワード)
- Animals / Antibodies, Bacterial / Bacteroidaceae Infections / Disease Models, Animal / Enzyme-Linked Immunosorbent Assay / Histocytochemistry / Immunity, Cellular / Immunity, Humoral / Immunoglobulin G / Injections, Subcutaneous / Interleukin-6 / Liver / Male / Mice / Mice, Inbred BALB C / Periodontitis / Porphyromonas gingivalis / Skin
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21880208
- ● Summary page in Scopus @ Elsevier: 2-s2.0-80052897323
(PubMed: 21880208, Elsevier: Scopus) 村井 治, 成石 浩司, 佐々木 大輔, 大川 義人, 八重柏 隆, 國松 和司 :
臨床研究 医科歯科連携医療における歯周病原細菌に対する血清IgG抗体価検査の導入,
日本口腔検査学会雑誌, Vol.3, No.1, 36-41, 2011年.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1050845762641886336
(CiNii: 1050845762641886336) Noriko Sugi, Koji Naruishi, Chieko Kudo, Aya Hisaeda-Kako, Takayuki Kono, Hiroshi Maeda and Shogo Takashiba :
Prognosis of periodontitis recurrence after intensive periodontal treatment using examination of serum IgG antibody titer against periodontal bacteria.,
Journal of Clinical Laboratory Analysis, Vol.25, No.1, 25-32, 2011.- (要約)
- Chronic periodontitis is associated with systemic diseases such as atherosclerosis. In this study, we evaluated the efficacy of serum IgG antibody titer to periodontal bacteria for prognosis of periodontitis recurrence during supportive periodontal therapy (SPT) phase. The 139 patients during SPT phase were selected and divided to two groups as follows: "Stable" and "Recurrence" group at SPT phase for case-control study: "High IgG titer" and "Normal IgG titer" group before transition to SPT phase for cohort study. We examined whether clinical findings or serum IgG antibody titers to periodontal bacteria are risk factors for the development of periodontitis recurrence. Case-control study showed that there were significant differences between the stable and recurrence groups in age and number of teeth. The serum IgG antibody titer to Eikenella corrodens FDC1073, Porphyromonas gingivalis SU63, and Campylobacter rectus ATCC33238 was significantly higher in the recurrence group. Next, we found, that the recurrence ratio in the high IgG titer group to Gram-negative obligate anaerobe, Prevotella intermedia, Treponema denticola, and C. rectus was significantly higher than that of the normal IgG titer group. Taken together, serum IgG antibody titer test is useful in the prognosis of periodontitis recurrence during the SPT phase.
- (キーワード)
- Aged / Aging / Antibodies, Bacterial / Biological Markers / Case-Control Studies / Chronic Disease / Chronic Periodontitis / Cohort Studies / Dental Care / Dentition / Female / Gram-Negative Bacteria / Humans / Immunoglobulin G / Male / Middle Aged / Prognosis / Recurrence / Risk Factors
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1002/jcla.20381
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21254239
- ● Search Scopus @ Elsevier (PMID): 21254239
- ● Search Scopus @ Elsevier (DOI): 10.1002/jcla.20381
(DOI: 10.1002/jcla.20381, PubMed: 21254239) Osamu Murai, Koji Naruishi, Satoshi Ogihara, Nagisa Suwa, Satomi Kanazawa, Takashi Yaegashi, Yasunori Takeda and Kazushi Kunimatsu :
Cathepsin B, D, and L regulation in cyclosporin A-mediated gingival hyperplasia of a patient with sarcoidosis.,
Clinical Laboratory, Vol.57, No.7-8, 535-541, 2011.- (要約)
- Cyclosporin A (CsA) is an immunosuppressant with side effects including gingival hyperplasia. Sarcoidosis is a systemic disease characterized by granulomas. Here, we report on a rare case of sarcoidosis with gingival hyperplasia to clarify whether clinical observation corresponds to in vitro results. Gingival fibroblasts (HGFs) were isolated from healthy gingiva and cultured with CsA. Total RNA was collected and expression of mRNAs examined using semi-quantitative RT-PCR analysis. Cathepsin B, D, and L expression in overgrown gingiva of the patient was examined by immunohistochemistry. Cathepsin D, L, and vascular endothelial growth factor (VEGF)165 mRNA were markedly suppressed in CsA-treated HGFs, whereas cathepsin B, matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA were not reduced. Next, the decrease of cathepsin B and L expression in enlarged gingiva was observed, whereas an increase of cathepsin D expression was observed. Clinically, the enlarged gingival lesions were fully resolved by performing oral infection control. Cathepsins regulation might be an important factor in the development of CsA-mediated gingival hyperplasia.
- (キーワード)
- Adrenal Cortex Hormones / Bacteroidaceae Infections / Cathepsin B / Cathepsin D / Cathepsin L / Cyclosporine / Dental Scaling / Drug Therapy, Combination / Enzyme Induction / Female / Gene Expression Regulation / Gingival Hyperplasia / Gingivitis / Humans / Immunocompromised Host / Immunosuppressive Agents / Matrix Metalloproteinase 1 / Middle Aged / Oral Hygiene / Porphyromonas gingivalis / Sarcoidosis / Tissue Inhibitor of Metalloproteinase-1 / Treponema denticola / 血管内皮増殖因子 (vascular endothelial growth factor)
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21888018
- ● Search Scopus @ Elsevier (PMID): 21888018
(PubMed: 21888018) 犬伏 順也, 畑中 加珠, 安田 多賀子, 成石 浩司, 大槻 秀彦, 高柴 正悟 :
サポーティブペリオドンタルセラピー期における塗布用ブラシ一体型一般用歯周病薬の臨床的および細菌学的な効果,
日本歯周病学会会誌, Vol.52, No.3, 225-238, 2010年.- (要約)
- サポーティブペリオドンタルセラピー(SPT)期における歯周組織の安定には, 定期的な専門的管理に加え, 患者自身の日々のプラークコントロールが重要である.今回我々は, 患者によるプラークコントロールを強化する目的で, 殺菌作用のある塩化セチルピリジニウム, 抗炎症効果のあるグリチルリチン酸二カリウムおよび組織創傷治癒効果をもつアラントインの3種の薬効成分を配合した薬剤をタフトブラシと一体化した塗布用ブラシ一体型歯周病薬(MC1)を開発した.本研究では, SPT期の歯周組織の維持・改善に対するMC1の有効性を臨床的および細菌学的指標を用いて評価した.<BR>本研究は, SPT期の慢性歯周炎患者を対象とした二重盲検法にて実施した.被験者として61名が参加し(試験群 : 27名, プラセボ群 : 28名, 脱落 : 6名), 4 mm以上の歯周ポケットを残す臼歯2歯の辺縁歯肉に, 1日2回12週間, MC1を塗布した.MC1の効果は, ベースライン時, 6および12週間目の3時点について, 臨床指標(PPD, BOP, PCR, GIおよびGCF量), および細菌学的指標(GCF中の総菌数, <I>Porphyromonas gingivalis</I>, <I>Tannerella forsythia </I>および<I>Treponema denticola</I>)を算出し, 統計学的に群間比較して検討した.<BR>PCRを除く全ての臨床指標は2群ともに経時的に有意に改善した.特に試験群では, GIおよびGCF量が早期に改善する傾向にあった.一方, 5mm以上の歯周ポケットを有する部位において, 試験群では調べた3菌種すべての菌数が, プラセボ群よりも有意に減少した.<BR>以上のことから, MC1はSPT期の慢性歯周炎患者の病状安定において, 臨床的および細菌学的に有効であることが示唆された.<BR>日本歯周病学会会誌(日歯周誌)52(3) : 225-238, 2010
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- ● Publication site (DOI): 10.2329/perio.52.225
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- ● CiNii @ 国立情報学研究所 (CRID): 1390001204411451008
- ● Search Scopus @ Elsevier (DOI): 10.2329/perio.52.225
(DOI: 10.2329/perio.52.225, CiNii: 1390001204411451008) K Yamabe, H Maeda, S Kokeguchi, Y Soga, M Meguro, Koji Naruishi, S Asakawa and S Takashiba :
Antigenic group II chaperonin in Methanobrevibacter oralis may cross-react with human chaperonin CCT.,
Molecular Oral Microbiology, Vol.25, No.2, 112-122, 2010.- (要約)
- Methanobrevibacter oralis is an archaeal species frequently isolated from sites of severe periodontitis. However, its pathogenic roles remain unclear. Here, we aimed to isolate group II chaperonin from M. oralis and examine its antigenicity. The genes encoding two chaperonin subunits (Cpn-1 and Cpn-2) were cloned from M. oralis using polymerase chain reaction and genome walking procedures. Recombinant proteins Cpn-1 and Cpn-2 were generated, and the reactivities of sera from patients with periodontitis were examined by Western immunoblotting. The open reading frames of Cpn-1 and Cpn-2 genes consisted of 1641 and 1614 base pairs, respectively. Putative ATP-binding domains conserved among the chaperonin family were observed in both genes. The deduced amino acid sequences of the two genes showed 28.8-40.0% identity to each of the subunits of human CCT (CCT1-8). Thirty and 29 of 36 patients' sera reacted with the recombinant Cpn-1 and recombinant Cpn-2, respectively. Western immunoblotting using antiserum against human CCT subunits indicated that anti-CCT3 and anti-CCT8 antibodies recognized recombinant Cpn-1. In addition, anti-CCT1, CCT3, CCT6, and CCT8 antibodies recognized an antigen of approximately 60 kDa in M. oralis. The results suggested that the chaperonin subunits of M. oralis were antigenic molecules that were recognized by periodontitis patients and that may cross-react with human chaperonin CCT.
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- Antigens, Archaeal / Chaperonin Containing TCP-1 / Chromosome Walking / Conserved Sequence / Cross Reactions / DNA, Archaeal / Group II Chaperonins / Host-Pathogen Interactions / Humans / Methanobrevibacter / 歯周病 (periodontitis) / Protein Subunits / Recombinant Proteins / Sequence Alignment / Sequence Analysis, DNA
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- ● Publication site (DOI): 10.1111/j.2041-1014.2009.00548.x
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- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20331799
- ● Summary page in Scopus @ Elsevier: 2-s2.0-77949404707
(DOI: 10.1111/j.2041-1014.2009.00548.x, PubMed: 20331799, Elsevier: Scopus) Y Koide, H Maeda, K Yamabe, Koji Naruishi, T Yamamoto, S Kokeguchi and S Takashiba :
Rapid detection of mecA and spa by the loop-mediated isothermal amplification (LAMP) method.,
Letters in Applied Microbiology, Vol.50, No.4, 386-392, 2010.- (要約)
- The LAMP offers an alternative detection assay for mecA and spa with a great advantage of the rapidity.
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- Aged / Aged, 80 and over / Bacterial Proteins / Bacteriological Techniques / DNA, Bacterial / Dental Plaque / Humans / Limit of Detection / Methicillin-Resistant Staphylococcus aureus / Middle Aged / Nucleic Acid Amplification Techniques / Polymerase Chain Reaction / Sensitivity and Specificity / Staphylococcal Protein A
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- ● Publication site (DOI): 10.1111/j.1472-765X.2010.02806.x
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- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20149082
- ● Search Scopus @ Elsevier (PMID): 20149082
- ● Search Scopus @ Elsevier (DOI): 10.1111/j.1472-765X.2010.02806.x
(DOI: 10.1111/j.1472-765X.2010.02806.x, PubMed: 20149082) 小出 康史, 杉 典子, 向井 麻理子, 児玉 由佳, 竹本 奈奈, 大隅 満奈, 藤井 友利江, 成石 浩司, 高柴 正悟 :
臨床研究 周術期患者に対する口腔管理システムの樹立と評価,
日本口腔検査学会雑誌, Vol.2, No.1, 45-49, 2010年.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1050564287665095296
(CiNii: 1050564287665095296) Takemasa Maeda, Hiroshi Maeda, Kokoro Yamabe, Junji Mineshiba, Ichiro Tanimoto, Tadashi Yamamoto, Koji Naruishi, Susumu Kokeguchi and Shogo Takashiba :
Highly expressed genes in a rough-colony-forming phenotype of Aggregatibacter actinomycetemcomitans: implication of a mip-like gene for the invasion of host tissue.,
FEMS Immunology and Medical Microbiology, Vol.58, No.2, 226-236, 2009.- (要約)
- Aggregatibacter actinomycetemcomitans, a potent pathogen of periodontitis, typically grows as a rough and adherent colony on primary isolated cultures. The colony transforms into a smooth phenotype during repeated subculture. In this study, we aimed to identify highly expressed genes in the rough-colony-forming phenotype for isolation of host-induced genes. Using a cDNA-subtractive hybridization technique, three genes, homologous to a macrophage infectivity potentiator gene (mip), peroxiredoxin gene (prx) and outer membrane protein gene (ompA), were identified. The expression levels of these genes in the rough-colony-forming phenotype were 4-10-fold higher as compared with the smooth-colony-forming phenotype. Attention was focused on the mip-like gene, and a recombinant protein and a deficient mutant were constructed. The recombinant protein reacted with sera from patients with periodontitis, suggesting the production of the Mip-like protein in periodontal lesions. Viable quantitative invasion assay demonstrated that the viable cell counts of the wild-type strain that invaded HeLa cells were more than fourfold as compared with the mip-deficient mutant. The expression of the mip-like gene, prx-like gene and ompA-like gene may be enhanced in the host, and the mip-like gene may play an important role in the infection of A. actinomycetemcomitans, especially in its invasion of the epithelium.
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- Antibodies, Bacterial / Bacterial Proteins / Colony Count, Microbial / Epithelial Cells / Gene Deletion / Gene Expression Regulation, Bacterial / HeLa Cells / Humans / Nucleic Acid Hybridization / Pasteurellaceae / 歯周病 (periodontitis) / Recombinant Proteins / 病原因子 (virulence factor) / Virulence Factors
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- ● Publication site (DOI): 10.1111/j.1574-695X.2009.00624.x
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- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19903198
- ● Search Scopus @ Elsevier (PMID): 19903198
- ● Search Scopus @ Elsevier (DOI): 10.1111/j.1574-695X.2009.00624.x
(DOI: 10.1111/j.1574-695X.2009.00624.x, PubMed: 19903198) Masami Watanabe, Guang Yang, Guangwen Cao, A Salahaldin Tahir, Koji Naruishi, Ken-Ichi Tabata, Abdel Elmoataz Fattah, Kartik Rajagopalan, L Terry Timme, Sanghee Park, Shinji Kurosaka, Kohei Edamura, Ryuta Tanimoto, J Francesco Demayo, A Alexei Goltsov and C Timothy Thompson :
Functional analysis of secreted caveolin-1 in mouse models of prostate cancer progression.,
Molecular Cancer Research : MCR, Vol.7, No.9, 1446-1455, 2009.- (要約)
- Previously, we reported that caveolin-1 (cav-1) is overexpressed in metastatic prostate cancer and that virulent prostate cancer cells secrete biologically active cav-1. We also showed that cav-1 expression leads to prosurvival activities through maintenance of activated Akt and that cav-1 is taken up by other cav-1-negative tumor cells and/or endothelial cells, leading to stimulation of angiogenic activities through PI-3-K-Akt-eNOS signaling. To analyze the functional consequences of cav-1 overexpression on the development and progression of prostate cancer in vivo, we generated PBcav-1 transgenic mice. Adult male PBcav-1 mice showed significantly increased prostatic wet weight and higher incidence of epithelial hyperplasia compared with nontransgenic littermates. Increased immunostaining for cav-1, proliferative cell nuclear antigen, P-Akt, and reduced nuclear p27(Kip1) staining occurred in PBcav-1 hyperplastic prostatic lesions. PBcav-1 mice showed increased resistance to castration-induced prostatic regression and elevated serum cav-1 levels compared with nontransgenic littermates. Intraprostatic injection of androgen-sensitive, cav-1-secreting RM-9 mouse prostate cancer cells resulted in tumors that were larger in PBcav-1 mice than in nontransgenic littermates (P = 0.04). Tail vein inoculation of RM-9 cells produced significantly more experimental lung metastases in PBcav-1 males than in nontransgenic male littermates (P = 0.001), and in cav-1(+/+) mice than in cav-1(-/-) mice (P = 0.041). Combination treatment with surgical castration and systemic cav-1 antibody dramatically reduced the number of experimental metastases. These experimental data suggest a causal association of secreted cav-1 and prostate cancer growth and progression.
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- 分散分析 (analysis of variance) / Androgen-Binding Protein / Androgens / Animals / Caveolin 1 / Cell Line, Tumor / Disease Models, Animal / Disease Progression / Lung Neoplasms / Male / Mice / Mice, Transgenic / Neoplasm Metastasis / Neoplasm Transplantation / Orchiectomy / Promoter Regions, Genetic / Prostatic Hyperplasia / Prostatic Neoplasms / Proto-Oncogene Proteins c-akt / 血管内皮増殖因子 (vascular endothelial growth factor)
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- ● Publication site (DOI): 10.1158/1541-7786.MCR-09-0071
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- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19737975
- ● Search Scopus @ Elsevier (PMID): 19737975
- ● Search Scopus @ Elsevier (DOI): 10.1158/1541-7786.MCR-09-0071
(DOI: 10.1158/1541-7786.MCR-09-0071, PubMed: 19737975) Y-S Ho, M-T Lai, S-J Liu, C-T Lin, Koji Naruishi, S Takashiba and H-H Chou :
Porphyromonas gingivalis fimbriae-dependent interleukin-6 autocrine regulation by increase of gp130 in endothelial cells.,
Journal of Periodontal Research, Vol.44, No.4, 550-556, 2009.- (要約)
- Our findings indicate that P. gingivalis fimbriae are important factors in the autocrine regulation of IL-6, by increasing gp130 in endothelial cells.
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- Autocrine Communication / Calcium-Calmodulin-Dependent Protein Kinases / Cells, Cultured / Coculture Techniques / Cytokine Receptor gp130 / Endothelial Cells / Endothelium, Vascular / Enzyme Inhibitors / Fimbriae Proteins / Fimbriae, Bacterial / フラボノイド (flavonoids) / Humans / Interleukin-6 / Mutation / NF-kappa B / Nitriles / Pili, Sex / Porphyromonas gingivalis / Sulfones / Umbilical Veins
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- ● Publication site (DOI): 10.1111/j.1600-0765.2008.01150.x
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- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19438975
- ● Search Scopus @ Elsevier (PMID): 19438975
- ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2008.01150.x
(DOI: 10.1111/j.1600-0765.2008.01150.x, PubMed: 19438975) 工藤 値英子, 成石 浩司, 久松 綾, 新井 英雄, 前田 博史, 高柴 正悟 :
歯周病スクリーニング検査としての歯周病原細菌に対する指尖血漿IgG抗体価の有用性,
日本口腔検査学会雑誌, Vol.1, No.1, 13-19, 2009年.- (キーワード)
- 歯周炎 (periodontal disease) / screening test / serum (plasma) IgG antibody titer / ELISA / mail testing
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1050001337711668224
(CiNii: 1050001337711668224) K Tabata, M Watanabe, Koji Naruishi, K Edamura, T Satoh, G Yang, E Fattah Abdel, J Wang, A Goltsov, D Floryk, D S Soni, D Kadmon and C T Thompson :
Therapeutic effects of gelatin matrix-embedded IL-12 gene-modified macrophages in a mouse model of residual prostate cancer.,
Prostate Cancer and Prostatic Diseases, Vol.12, No.3, 301-309, 2008.- (要約)
- We evaluated the potential use of intraoperative gelatin matrix hemostatic sealant (GMHS; FloSeal; Baxter Healthcare) embedded with macrophages (Mphi) transduced with murine interleukin (IL)-12 recombinant adenoviral vector (G/Mphi/AdmIL-12) for prevention of recurrence of prostate cancer following radical prostatectomy. Application of G/Mphi/AdmIL-12 resulted in significant suppression of tumor growth and spontaneous lung metastases, a statistically significant survival advantage of the G/Mphi/AdmIL-12-treated animals, more efficient trafficking of Mphi to lymph nodes draining from the prostate and generation of systemic natural killer cell activity and tumor-specific cytolytic T lymphocyte responses compared to the controls in a preclinical mouse model of residual prostate cancer. Our data recommend this treatment as a novel adjuvant for prevention of local recurrence of prostate cancer following radical prostatectomy.
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- Adenoviridae / Animals / Cell Movement / Cell Survival / Disease Models, Animal / Gelatin / Genetic Therapy / Hemostatics / Interleukin-12 / Macrophages / Male / Mice / Prostatic Neoplasms
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- ● Publication site (DOI): 10.1038/pcan.2008.57
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- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19104507
- ● Search Scopus @ Elsevier (PMID): 19104507
- ● Search Scopus @ Elsevier (DOI): 10.1038/pcan.2008.57
(DOI: 10.1038/pcan.2008.57, PubMed: 19104507) Tomoko Yamaguchi, Koji Naruishi, Hideo Arai, Fusanori Nishimura and Shogo Takashiba :
IL-6/sIL-6R enhances cathepsin B and L production via caveolin-1-mediated JNK-AP-1 pathway in human gingival fibroblasts.,
Journal of Cellular Physiology, Vol.217, No.2, 423-432, 2008.- (要約)
- Interleukin (IL)-6 has an important role in inflammatory diseases. Lysosomal enzymes cathepsins are widely expressed as cysteine proteases regulating inflammatory process. Caveolin-1 (Cav-1) is a scaffolding/regulatory membrane protein that interacts with signaling molecules. In this study, we investigated the role of Cav-1 on (1) the productivity, and (2) the enzymatic activity of cathepsin B and L in human gingival fibroblasts (HGFs) treated with IL-6 in the presence of soluble form of IL-6 receptor (sIL-6R). At first, we established the siRNA-mediated Cav-1 down-regulating in vitro systems by transient transfection of Cav-1 siRNA. The siRNA-mediated Cav-1 down-regulated cells were treated with IL-6/sIL-6R for indicated times. Then, cell lysates were collected, and examined the IL-6-induced signaling pathway, cathepsin B and L production, and measurement of cathepsins activity. To investigate the cathepsin L activity, cathepsin-(B + L) activity was measured after pretreatment with CA-074Me, a specific inhibitor for cathepsin B. We found that IL-6/sIL-6R enhanced significantly both production and activity of cathepsin B and L in HGFs. Interestingly, IL-6-mediated phosphorylation of both p44/42 MAPK and JNK was dramatically suppressed in Cav-1 down-regulated HGFs treated with IL-6/sIL-6R. In addition, both production and activity of cathepsin B and L were also significantly suppressed. Importantly, we demonstrated that JNK inhibition, but not p44/42 MAPK inhibition, significantly diminished IL-6/sIL-6R-induced cathepsin B and L production. Taken together, we concluded that IL-6/sIL-6R enhances cathepsin B and L production via IL-6/sIL-6R-mediated Cav-1-JNK-AP-1 pathway in HGFs. Our findings indicate that Cav-1 might be a therapeutic target for IL-6-mediated tissue degradation in periodontitis.
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- Anthracenes / Cathepsin B / Cathepsin L / Cathepsins / Caveolin 1 / Cells, Cultured / Cysteine Endopeptidases / Dipeptides / Fibroblasts / フラボノイド (flavonoids) / Gingiva / Humans / Interleukin-6 / JNK Mitogen-Activated Protein Kinases / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / 歯周病 (periodontitis) / リン酸化 (phosphorylation) / Protease Inhibitors / Protein Kinase Inhibitors / RNA Interference / RNA, Small Interfering / Receptors, Interleukin-6 / Recombinant Proteins / シグナル伝達 (signal transduction) / Time Factors / Transcription Factor AP-1 / Transfection / Up-Regulation
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- ● Publication site (DOI): 10.1002/jcp.21517
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- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18543249
- ● Search Scopus @ Elsevier (PMID): 18543249
- ● Search Scopus @ Elsevier (DOI): 10.1002/jcp.21517
(DOI: 10.1002/jcp.21517, PubMed: 18543249) 福家 教子, 苅田 典子, 熊崎 洋平, 成石 浩司, 大西 典子, 明貝 文夫, 岩本 義博, 新井 英雄, 高柴 正悟 :
サポーティブペリオドンタルセラピーによる歯周炎の再発防止と進行抑制の効果に関する統計学的検討,
岡山歯学会雑誌, Vol.27, No.2, 105-113, 2008年. Guang Yang, L Terry Timme, Koji Naruishi, Tetsuo Fujita, Abdel El Moataz Fattah, Guangwen Cao, Kartik Rajagopalan, Kartik Rajocopolan, D Luan Troung and C Timothy Thompson :
Mice with cav-1 gene disruption have benign stromal lesions and compromised epithelial differentiation.,
Experimental and Molecular Pathology, Vol.84, No.2, 131-140, 2007.- (要約)
- Caveolin-1 (cav-1) is a major structural protein of caveolae, small invaginations of the plasma membrane that integrate and regulate signaling pathways involved in cell growth and differentiation. We previously generated a genetically engineered mice that are homozygous for a null mutation in exon 2 of cav-1 and documented increased incidence of urolithiasis in young male cav-1(-/-) mice. We attributed this, in part, to improper localization of plasma membrane calcium/calmodulin-dependent calcium ATPase in the distal convoluted tubules of the kidney. To document pathologies related to cav-1 function, we maintained cav-1(-/-) and control cav-1(+/+) mice for an extended time period. We report here that cav-1(-/-) mice demonstrate organ-specific growth-related disorders in stromal cells that normally have high levels of cav-1 expression. In many of these organs, epithelial cell growth/differentiation abnormalities were also observed, yet in most of these sites the epithelial cells normally express low to non-detectable levels of cav-1. We propose that loss of cav-1 function in stromal cells of various organs directly leads to a disorganized stromal compartment that, in turn, indirectly promotes abnormal growth and differentiation of adjacent epithelium.
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- Animals / Biological Markers / Caveolin 1 / 細胞増殖·分化 (cell proliferation and differentiation) / Epithelial Cells / Female / Gene Expression Regulation / Gene Silencing / Genitalia / Keratins / Longevity / Lung / Male / Mammary Glands, Animal / Mice / Mice, Inbred C57BL / ノックアウトマウス (knockout mice) / Pancreas / Spleen / Stromal Cells / Urinary Bladder
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- ● Publication site (DOI): 10.1016/j.yexmp.2007.08.004
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- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18358473
- ● Search Scopus @ Elsevier (PMID): 18358473
- ● Search Scopus @ Elsevier (DOI): 10.1016/j.yexmp.2007.08.004
(DOI: 10.1016/j.yexmp.2007.08.004, PubMed: 18358473) Kazuhiro Omori, Koji Naruishi, Tomoko Yamaguchi, Shun-Ai Li, Mayumi Yamaguchi-Morimoto, Kaori Matsuura, Hideo Arai, Kohji Takei and Shogo Takashiba :
cAMP-response element binding protein (CREB) regulates cyclosporine-A-mediated down-regulation of cathepsin B and L synthesis.,
Cell and Tissue Research, Vol.330, No.1, 75-82, 2007.- (要約)
- Cyclosporin A (CsA) is an immunosuppressant with severe side effects including gingival overgrowth. We have previously reported that CsA impairs the activity of the lysosomal enzymes cathepsin B and L in human gingival fibroblasts (HGFs). Here, we have examined the effects of CsA on the DNA-binding activity of the cyclic AMP response element-binding protein (CREB) and cell viability, and the effects of CREB on cathepsin B and L synthesis and activity in HGFs. We have confirmed that CsA down-regulates cathepsin B and L synthesis. Further, CsA has no effect on cell viability and dramatically impairs CREB-DNA binding activity. Importantly, the synthesis of cathepsin B and L is down-regulated, and their activity is also significantly impaired in HGFs transfected with plasmid expressing dominant-negative CREB. These results suggest that CREB is essential for the CsA-mediated down-regulation of cathepsin B and L synthesis in HGFs.
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- CREB-Binding Protein / Cathepsin B / Cathepsin L / Cathepsins / Cell Survival / Cyclosporine / Cysteine Endopeptidases / Down-Regulation / Fibroblasts / Gingiva / Humans / Lysosome-Associated Membrane Glycoproteins / Lysosomes / Transfection
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- ● Publication site (DOI): 10.1007/s00441-007-0457-8
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17724614
- ● Search Scopus @ Elsevier (PMID): 17724614
- ● Search Scopus @ Elsevier (DOI): 10.1007/s00441-007-0457-8
(DOI: 10.1007/s00441-007-0457-8, PubMed: 17724614) H Wang, G Yang, L T Timme, T Fujita, Koji Naruishi, A Frolov, K M Brenner, D Kadmon and C T Thompson :
IL-12 gene-modified bone marrow cell therapy suppresses the development of experimental metastatic prostate cancer.,
Cancer Gene Therapy, Vol.14, No.10, 819-827, 2007.- (要約)
- To investigate the immunomodulatory effects of interleukin-12 (IL-12) for treatment of metastatic prostate cancer, we administered adult bone marrow cells (BMC) that were genetically modified by retroviral vector-mediated IL-12 gene transduction in an experimental mouse model of prostate cancer metastasis. This therapy produced significant anti-metastatic effects in bone and lung and prolonged animal survival. Flow cytometric analysis indicated donor BMC could effectively home to bone and lung after treatment. Intensive infiltration of CD4 and CD8T cells in lung metastases and increased systemic natural killer and cytotoxic T lymphocyte activities indicated induction of a significant anti-metastatic immune response after treatment with IL-12 transduced BMC. Our results demonstrate the therapeutic potential of gene-modified BMC gene therapy.
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- Animals / Bone Marrow Cells / Bone Neoplasms / Disease Models, Animal / 遺伝子発現 (gene expression) / Genetic Vectors / Green Fluorescent Proteins / Interleukin-12 / Killer Cells, Natural / Lung Neoplasms / Male / Mice / Prostatic Neoplasms / Retroviridae / Survival Rate / T-Lymphocytes, Cytotoxic / Transduction, Genetic
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- ● Publication site (DOI): 10.1038/sj.cgt.7701069
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- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17627292
- ● Search Scopus @ Elsevier (PMID): 17627292
- ● Search Scopus @ Elsevier (DOI): 10.1038/sj.cgt.7701069
(DOI: 10.1038/sj.cgt.7701069, PubMed: 17627292) Arias Zulema Rosalia Martinez, Koji Naruishi, Keisuke Yamashiro, Fumio Myokai, Teruo Yamada, Kaori Matsuura, Naoko Namba, Hideo Arai, Junzo Sasaki, Yoshimitsu Abiko and Shogo Takashiba :
Gene profiles during root canal treatment in experimental rat periapical lesions.,
Journal of Endodontics, Vol.33, No.8, 936-943, 2007.- (要約)
- The purpose of this study was to profile gene expression in periapical lesions during root canal treatment (RCT). Periapical lesions were induced experimentally by exposing the pulp in Sprague-Dawley rats. After 3 wk, the animals received root canal filling (RCF) and were sacrificed 1 or 4 wk later. From the periapical tissues, total RNA was extracted and processed for cDNA-microarray analysis. The lesions were histologically and radiographically confirmed to expand 4 wk after pulp exposure (inflammation phase) and to stabilize 4 wk after RCF (healing phase). In approximately 30,000 genes on the microarray, 203 genes were up-regulated to more than 5-fold (e.g., IL-1beta), and 864 genes were down-regulated to less than 20% of baseline level (e.g., caspase 8) in inflammation phase. Compared with inflammation phase, we found that 133 genes were up-regulated (e.g., IL-1alpha) and 50 genes were down-regulated (e.g., defensin alpha5) in healing phase. Corresponding to the gene expression profiles, accumulation of IL-1alpha and IL-1beta was observed in the periapical lesions by immunohistochemistry. These gene profiles might be useful in diagnosing the healing process of periapical lesions.
- (キーワード)
- Animals / Disease Models, Animal / Down-Regulation / Gene Expression Profiling / Immunoenzyme Techniques / Interleukin-1 / Male / Oligonucleotide Array Sequence Analysis / Periapical Periodontitis / Rats / Rats, Sprague-Dawley / Reverse Transcriptase Polymerase Chain Reaction / Root Canal Therapy / Up-Regulation / Wound Healing
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1016/j.joen.2007.04.016
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17878078
- ● Search Scopus @ Elsevier (PMID): 17878078
- ● Search Scopus @ Elsevier (DOI): 10.1016/j.joen.2007.04.016
(DOI: 10.1016/j.joen.2007.04.016, PubMed: 17878078) T Fujita, L T Timme, K Tabata, Koji Naruishi, N Kusaka, M Watanabe, E Abdelfattah, X J Zhu, C Ren, C Ren, G Yang, A Goltsov, H Wang, T M Vlachaki, S B Teh, B E Butler and C T Thompson :
Cooperative effects of adenoviral vector-mediated interleukin 12 gene therapy with radiotherapy in a preclinical model of metastatic prostate cancer.,
Gene Therapy, Vol.14, No.3, 227-236, 2006.- (要約)
- We investigated the potential benefits of combining adenoviral vector mediated in situ interleukin-12 (AdmIL-12) gene therapy with radiation therapy (XRT) to enhance therapeutic efficacy. In a metastatic mouse prostate cancer cell line, 178-2 BMA, AdmIL-12+XRT demonstrated enhanced therapeutic activities in vitro as determined by clonogenic survival, apoptosis, and mIL-12 levels. At the molecular level, increased expression of tumor necrosis factor-alpha mRNA was specific for the combined therapy. In a subcutaneous 178-2 BMA in vivo model, the combination of AdmIL-12+XRT produced statistically significant tumor growth suppression compared to control vector Adbetagal, Adbetagal XRT, or AdmIL-12 as monotherapy. In addition, significant prolongation of survival was demonstrated for the combination of AdmIL-12+XRT. The combination of AdmIL-12+XRT significantly suppressed both spontaneous and pre-established lung metastases, and led to a prolonged elevation of serum IL-12 and significantly increased natural killer (NK) activities. Importantly, in vivo depletion of NK cells resulted in significant attenuation of the antimetastatic activities of AdmIL-12 alone or AdmIL-12+XRT. These combined effects suggest that AdIL-12 gene therapy together with radiotherapy may achieve maximal tumor control (both local and systemic) in selected prostate cancer patients via radio-gene therapy induced local cytotoxicity and local and systemic antitumor immunity.
- (キーワード)
- Adenoviridae / Animals / Cell Line, Tumor / Combined Modality Therapy / Genetic Therapy / Genetic Vectors / Humans / Injections, Intralesional / Interleukin-12 / Killer Cells, Natural / Lung Neoplasms / Male / Mice / Mice, Mutant Strains / Prostatic Neoplasms / Transduction, Genetic / Tumor Necrosis Factor-alpha
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1038/sj.gt.3302788
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17024109
- ● Search Scopus @ Elsevier (PMID): 17024109
- ● Search Scopus @ Elsevier (DOI): 10.1038/sj.gt.3302788
(DOI: 10.1038/sj.gt.3302788, PubMed: 17024109) Nobuyuki Shiomi, Fumio Myokai, Koji Naruishi, Kosuke Oyaizu, Kyoko Senoo, Tomoko Yamaguchi, Salomon Amar and Shogo Takashiba :
Cloning and characterization of lipopolysaccharide-induced tumor necrosis factor alpha factor promoter.,
FEMS Immunology and Medical Microbiology, Vol.47, No.3, 360-368, 2006.- (要約)
- We have recently identified lipopolysaccharide tumor-induced tumor necrosis factor alpha factor (LITAF) as a novel transcription factor controlling necrosis factor (TNF)-alpha expression in the human monocytic cell line, THP-1. To characterize the human (h) LITAF promoter, we isolated a 1.2-kb DNA fragment and followed this by a screening of human genomic DNA with a hLITAF cDNA probe. A 34-bp sequence domain located from nucleotides -74 to -43 in the hLITAF promoter exhibited the highest basal reporter gene activity; however, the activity was not elevated by lipopolysaccharide (LPS) stimulation. The sequence domain included a consensus sequence for hepatocyte nuclear factor (HNF)-3alpha, regulating the transcription of many kinds of genes. Interestingly, the DNA sequence position between -542 and -538 in the hLITAF promoter contained the CTCCC motif, which has been reported to act as a specific binding site for hLITAF protein. Electrophoretic mobility shift assays demonstrated that LPS induced the binding of THP-1 nuclear factors to a 22 bp probe containing the CTCCC motif. In addition, hLITAF mRNA and nuclear hLITAF protein increased significantly in the THP-1 cells immediately after LPS stimulation. These results suggest that the consensus sequence for HNF-3alpha, or a nuclear binding protein to the CTCCC motif, may play an important role in regulating LPS-dependent LITAF transcription.
- (キーワード)
- 5' Flanking Region / Base Sequence / Binding Sites / Cell Line, Tumor / Cell Nucleus / Cloning, Molecular / Consensus Sequence / DNA / Humans / Kinetics / Lipopolysaccharides / Molecular Sequence Data / Nuclear Proteins / Oligonucleotides / Promoter Regions, Genetic / RNA, Messenger / Transcription Factors / Transcription Initiation Site / Transcription, Genetic
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1111/j.1574-695X.2006.00094.x
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16872372
- ● Search Scopus @ Elsevier (PMID): 16872372
- ● Search Scopus @ Elsevier (DOI): 10.1111/j.1574-695X.2006.00094.x
(DOI: 10.1111/j.1574-695X.2006.00094.x, PubMed: 16872372) Koji Naruishi, L T Timme, N Kusaka, T Fujita, G Yang, A Goltsov, T Satoh, X Ji, W Tian, E Abdelfattah, T Men, M Watanabe, K Tabata and C T Thompson :
Adenoviral vector-mediated RTVP-1 gene-modified tumor cell-based vaccine suppresses the development of experimental prostate cancer.,
Cancer Gene Therapy, Vol.13, No.7, 658-663, 2006.- (要約)
- We previously identified a novel p53 target gene, RTVP-1, that possesses unique cytotoxic and immunostimulatory activities which make it potentially useful for cancer gene therapy. To test the therapeutic potential of RTVP-1 in a gene-modified tumor cell-based vaccine model, we used an adenoviral vector capable of efficient transduction and expression of RTVP-1 (AdRTVP-1), together with a highly metastatic mouse prostate cancer cell line (178-2 BMA). A vaccine was prepared with 178-2 BMA cells transduced with AdRTVP-1 or a control adenoviral vector expressing beta-galactosidase (Adbetagal). After irradiation of the cells, syngeneic 129/Sv mice were vaccinated three times at weekly intervals. After 3 weeks, they were challenged with orthotopic 178-2 BMA cells. After 21 days, fewer than 60% of the RTVP-1-cell-vaccinated mice developed tumors compared to 100% of the control mice. The RTVP-1-cell vaccine significantly reduced primary tumor wet weight compared with control Adbetagal-cell vaccine (P<0.0001 at 7 and 14 days). Experimental metastasis to lung was also significantly reduced (P=0.0377), and survival significantly increased (P=0.0002). In addition, significantly increased NK and CTL activities were demonstrated in the AdRTVP-1-cell-vaccinated mice. These findings indicate that RTVP-1 gene-modified cell-based vaccines may be useful in the prevention of recurrent prostate cancer.
- (キーワード)
- Adenoviridae / Animals / Cancer Vaccines / Cell Line, Tumor / Humans / Male / Mice / Neoplasm Proteins / Neoplasms, Experimental / Nerve Tissue Proteins / Prostatic Neoplasms / Transduction, Genetic
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1038/sj.cgt.7700919
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16485011
- ● Search Scopus @ Elsevier (PMID): 16485011
- ● Search Scopus @ Elsevier (DOI): 10.1038/sj.cgt.7700919
(DOI: 10.1038/sj.cgt.7700919, PubMed: 16485011) Tetsuo Fujita, S Bin Teh, L Terry Timme, Wei-Yuan Mai, Takefumi Satoh, Nobuyuki Kusaka, Koji Naruishi, Abdel Elmoataz Fattah, Estuardo Aguilar-Cordova, Brian E Butler and C Timothy Thompson :
Sustained long-term immune responses after in situ gene therapy combined with radiotherapy and hormonal therapy in prostate cancer patients.,
International Journal of Radiation Oncology*Biology*Physics, Vol.65, No.1, 84-90, 2006.- (要約)
- Sustained long-term (up to 8 to 12 months) systemic T-cell responses were noted after combined radio-gene-hormonal therapy for prostate cancer. Prolonged use of hormonal therapy does not suppress this response. These results suggest the potential for sustained activation of cell-mediated immune responses against cancer.
- (キーワード)
- Acyclovir / Adenoviridae / Aged / Aged, 80 and over / Androgen Antagonists / Antiviral Agents / CD4-Positive T-Lymphocytes / CD8-Positive T-Lymphocytes / Combined Modality Therapy / Genetic Therapy / Humans / Immunity, Cellular / Killer Cells, Natural / Male / Middle Aged / Prostatic Neoplasms / Radiotherapy, Intensity-Modulated / Thymidine Kinase / Valine
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1016/j.ijrobp.2005.11.009
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16472937
- ● Search Scopus @ Elsevier (PMID): 16472937
- ● Search Scopus @ Elsevier (DOI): 10.1016/j.ijrobp.2005.11.009
(DOI: 10.1016/j.ijrobp.2005.11.009, PubMed: 16472937) Mayumi Yamaguchi, Koji Naruishi, Hisa Yamada-Naruishi, Kazuhiro Omori, Fusanori Nishimura and Shogo Takashiba :
Long-term cyclosporin A exposure suppresses cathepsin-B and -L activity in gingival fibroblasts.,
Journal of Periodontal Research, Vol.39, No.5, 320-326, 2004.- (要約)
- The decreased ability of protein degradation by not only cathepsin-L but also cathepsin-B is, at least, one of the several factors developing the cyclosporin A-induced gingival overgrowth.
- (キーワード)
- Cathepsin B / Cathepsin L / Cathepsins / Cell Division / Cells, Cultured / Cyclosporine / Cysteine Endopeptidases / Cysteine Proteinase Inhibitors / Fibroblasts / Gingiva / Humans / Immunosuppressive Agents / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction / Time Factors
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1111/j.1600-0765.2004.00746.x
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15324353
- ● Search Scopus @ Elsevier (PMID): 15324353
- ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2004.00746.x
(DOI: 10.1111/j.1600-0765.2004.00746.x, PubMed: 15324353) Milan Petelin, Koji Naruishi, Nobuyuki Shiomi, Junji Mineshiba, Hideo Arai, Fusanori Nishimura, Shogo Takashiba and Yoji Murayama :
Systemic up-regulation of sTNFR2 and IL-6 in Porphyromonas gingivalis pneumonia in mice.,
Experimental and Molecular Pathology, Vol.76, No.1, 76-81, 2004.- (要約)
- Aspiration pneumonia is a common cause of death in older people, and the pathophysiology is a chronic respiratory failure with a mild airway inflammation. In this study, we established a mild inflammatory pneumonia model using Porphyromonas gingivalis (Pg) pathogen-infected mice. It elucidated the effects of Pg-infected pneumonia on proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin-6 (IL-6), and IL-1beta production in both lung tissue and serum. We also elucidated production of soluble (s) TNF receptor (R) s, because TNF-alpha is considered to be a dominant inflammatory mediator. Lung TNF-alpha levels significantly increased at 2 h after infection, and rapidly returned to basal level at 24 h. Consistent with increase of TNF-alpha, remarkable increase of sTNFR2 but not sTNFR1 was detected in lung tissue from 2 to 72 h. Interestingly, sTNFR2/sTNFR1 ratio was significantly enhanced at 2 h in serum. In addition, lung IL-1beta and IL-6 levels also significantly increased from 2 to 24 h. Importantly, we found that IL-6 levels in serum reflected its local level. These results may suggest that systemically produced sTNFR2 and IL-6 could be a key role to modulate proinflammatory activities of TNF-alpha in Pg-induced lung inflammation simulated aspiration pneumonia.
- (キーワード)
- Animals / Antigens, CD / Bacteroidaceae Infections / Disease Models, Animal / Enzyme-Linked Immunosorbent Assay / Interleukin-1 / Interleukin-6 / Lung / Male / Mice / Mice, Nude / Pneumonia, Aspiration / Porphyromonas gingivalis / Receptors, Tumor Necrosis Factor / Receptors, Tumor Necrosis Factor, Type I / Receptors, Tumor Necrosis Factor, Type II / Tumor Necrosis Factor-alpha / Up-Regulation
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14738872
- ● Search Scopus @ Elsevier (PMID): 14738872
(PubMed: 14738872) Kazuhiro Omori, Koji Naruishi, Fusanori Nishimura, Hisa Yamada-Naruishi and Shogo Takashiba :
High glucose enhances interleukin-6-induced vascular endothelial growth factor 165 expression via activation of gp130-mediated p44/42 MAPK-CCAAT/enhancer binding protein signaling in gingival fibroblasts.,
The Journal of Biological Chemistry, Vol.279, No.8, 6643-6649, 2003.- (要約)
- Diabetic patients are susceptible to severe inflammatory periodontitis manifesting as swollen gingiva with bleeding, but the underlying mechanism is not well understood. Our purpose was to determine the effect of a high glucose (HG) condition on the interleukin-6/soluble interleukin-6 receptor (IL-6/sIL-6R)-induced activation of signaling and vascular endothelial growth factor (VEGF) expression in human gingival fibroblasts (HGFs). In this study, HGFs were cultured for at least two passages under a normal glucose (NG; 5.5 mM) condition or high glucose (25 mM) condition. Importantly, the HG condition significantly induced expression of gp130 mRNA in HGFs compared with levels in control cells. Consistent with the expression of its mRNA, the HG condition also increased the expression of gp130 protein, and phosphorylation of the tyrosine residue by gp130 was enhanced significantly by IL-6/sIL-6R stimulation. Furthermore, the HG condition enhanced the IL-6/sIL-6R-induced phosphorylation of p44/42 MAPK and led to subsequent activation of CCAAT/enhancer binding protein in nuclei. In contrast, there was no significant difference in phosphorylation of JNK between the HG and NG condition. Interestingly, HGFs increased IL-6/sIL-6R-induced VEGF165 mRNA expression and VEGF165 secretion under the HG condition compared with levels under the NG condition. In contrast, the induction of VEGF165 secretion was partially inhibited by PD98059 (selective p44/42 MAPK inhibitor) under the HG condition. In addition, the VEGF165 secretion was completely inhibited by the combination of PD98059 and SP600125 (JNK inhibitor). Our findings suggest that the HG condition indirectly increases VEGF expression via activation of gp130-mediated p44/42 MAPK-CCAAT/enhancer binding protein signaling in HGFs. Thus, elevated VEGF secretion in HGFs under the HG condition may play a role in the development of the severe periodontitis observed in diabetic patients.
- (キーワード)
- Blotting, Western / CCAAT-Enhancer-Binding Proteins / Cell Line / Cell Nucleus / Contactins / DNA (DNA) / DNA-Binding Proteins / Dose-Response Relationship, Drug / Enzyme Activation / Enzyme Inhibitors / Fibroblasts / フラボノイド (flavonoids) / Gingiva / グルコース (glucose) / Humans / Interleukin-6 / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinases / Models, Biological / Neural Cell Adhesion Molecules / リン酸化 (phosphorylation) / RNA, Messenger / Receptors, Interleukin-6 / Recombinant Proteins / Reverse Transcriptase Polymerase Chain Reaction / シグナル伝達 (signal transduction) / Time Factors / Tyrosine / 血管内皮増殖因子 (vascular endothelial growth factor)
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1074/jbc.M311688200
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14676217
- ● Search Scopus @ Elsevier (PMID): 14676217
- ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M311688200
(DOI: 10.1074/jbc.M311688200, PubMed: 14676217) Koji Naruishi, Fusanori Nishimura, Hisa Yamada-Naruishi, Kazuhiro Omori, Mayumi Yamaguchi and Shogo Takashiba :
C-jun N-terminal kinase (JNK) inhibitor, SP600125, blocks interleukin (IL)-6-induced vascular endothelial growth factor (VEGF) production: cyclosporine A partially mimics this inhibitory effect.,
Transplantation, Vol.76, No.9, 1380-1382, 2003.- (要約)
- Angiogenesis is a common complication of organ-transplant rejection. One of the primary responsible molecules for enhanced angiogenesis is vascular endothelial growth factor (VEGF). Activated protein (AP)-1 is considered to play a key role in the transcription of VEGF. c-jun N-terminal kinase (JNK), one of the MAP kinase family members, plays a critical role in AP-1 activation. Thus, we tested the effect of a novel JNK inhibitor, SP600125, on VEGF production in fibroblasts. SP600125 significantly suppressed interleukin (IL)-6-induced production of VEGF in cultured fibroblasts. Cyclosporine A (CsA), a known in vitro anti-angiogenic reagent, partially mimicked this suppression. In fact, CsA suppressed IL-6-induced phosphorylation of JNK. The results indicate that although both SP600125 and CsA are anti-angiogenic by inhibiting VEGF production by way of a JNK-dependent pathway, the inhibitory effect was much stronger with the novel inhibitor of JNK than with CsA.
- (キーワード)
- Anthracenes / Cells, Cultured / Cyclosporine / Enzyme Inhibitors / Fibroblasts / Gingiva / Humans / Interleukin-6 / JNK Mitogen-Activated Protein Kinases / Mitogen-Activated Protein Kinases / Neovascularization, Pathologic / リン酸化 (phosphorylation) / 血管内皮増殖因子 (vascular endothelial growth factor)
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1097/01.TP.0000085661.52980.95
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14627919
- ● Search Scopus @ Elsevier (PMID): 14627919
- ● Search Scopus @ Elsevier (DOI): 10.1097/01.TP.0000085661.52980.95
(DOI: 10.1097/01.TP.0000085661.52980.95, PubMed: 14627919) Fusanori Nishimura, Hisa Naruishi, Koji Naruishi, Teruo Yamada, Junzo Sasaki, Christoph Peters, Yasuo Uchiyama and Yoji Murayama :
Cathepsin-L, a key molecule in the pathogenesis of drug-induced and I-cell disease-mediated gingival overgrowth: a study with cathepsin-L-deficient mice.,
The American Journal of Pathology, Vol.161, No.6, 2047-2052, 2002.- (要約)
- Drug-induced gingival overgrowth, the chronic side effect of calcium antagonists, is frequently seen due to the increase in patients with hypertension, although the etiology of the disease is largely unknown. I-cell disease, which accompanies gingival overgrowth, is characterized by a deficiency in UDP-N-acetyl-glucosamine and is classified as one of the lysosomal storage diseases. Here, we hypothesized that a common mechanism may underlie the etiology of gingival overgrowth seen in patients treated with calcium antagonist and in patients with I-cell disease. A calcium antagonist, nifedipine, specifically suppressed cathepsin-L activity and mRNA expression, but not that of cathepsin-B in cultured gingival fibroblasts. The activity of cathepsin-L was suppressed up to 50% at 24 hours after treatment of the cells with the reagent. The selective suppression of cathepsin-L activity appeared not to be dependent on Ca(2+), since treatment of the cells with thapsigargin suppressed both cathepsin-B and -L activity. Mice deficient in the cathepsin-L gene manifested enlarged gingivae. Histological observation of the gingivae demonstrated typical features of acanthosis, a phenotype very similar to that of experimentally induced gingival overgrowth. Since cathepsin-L deficiency was reported to be associated with thickening of the skin, impaired cathepsin-L activity may play a key role in the establishment of skin and gingival abnormalities seen in I-cell disease. In addition, reduced cathepsin-L activity may play an important role in inducing drug-induced gingival overgrowth.
- (キーワード)
- Animals / カルシウムチャネル (calcium channel) / Calcium Channel Blockers / Cathepsin B / Cathepsin L / Cathepsins / Cells, Cultured / Cysteine Endopeptidases / Enzyme Inhibitors / Fibroblasts / Gingiva / Gingival Overgrowth / HeLa Cells / Humans / Lysosomes / Mice / ノックアウトマウス (knockout mice) / Mucolipidoses / Nifedipine / Thapsigargin
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1016/S0002-9440(10)64483-5
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12466121
- ● Search Scopus @ Elsevier (PMID): 12466121
- ● Search Scopus @ Elsevier (DOI): 10.1016/S0002-9440(10)64483-5
(DOI: 10.1016/S0002-9440(10)64483-5, PubMed: 12466121) Koji Naruishi, S Takashiba, F Nishimura, H H Chou, H Arai, H Yamada and Y Murayama :
Impairment of gingival fibroblast adherence by IL-6/sIL-6R.,
Journal of Dental Research, Vol.80, No.5, 1421-1424, 2001.- (要約)
- Interleukin-6 (IL-6) binds to human gingival fibroblasts (HGF) in the presence of a soluble form of IL-6 receptor (sIL-6R). We investigated the effects of IL-6 on the functions of HGF in the presence of sIL-6R. HGF changed their morphology from spindle-shaped to round, and detached from the culture dish by stimulation with IL-6/sIL-6R. In this condition, a signal transducer gp130 and a transcription factor Stat3 were phosphorylated, resulting in activation of transcription factors Stat3 and C/EBPbeta. Cytoskeletal beta-actin and adhesion molecule integrin-alpha5, a subunit of alpha5beta1 integrin (VLA-5), were found to possess potential binding domains for these transcription factors in their promoters. Accumulation of beta-actin and integrin-alpha5 mRNA decreased, contrary to the expectation of the induction of gene transcription. Furthermore, the decrease in their mRNAs was associated with reduced expression of both actin and VLA-5 proteins. These results suggest that the expression of VLA-5 and actin was down-regulated in HGF through an IL-6 signaling pathway, resulting in impairment of HGF adherence.
- (キーワード)
- Actins / Amino Acid Sequence / Blotting, Western / Cell Adhesion / Cells, Cultured / Contactins / DNA-Binding Proteins / Down-Regulation / Electrophoresis, Polyacrylamide Gel / Fibroblasts / Gingiva / Gingivitis / Humans / Interleukin-6 / Molecular Sequence Data / Neural Cell Adhesion Molecules / リン酸化 (phosphorylation) / Protein Binding / Receptors, Fibronectin / Receptors, Interleukin / Receptors, Interleukin-6 / Recombinant Fusion Proteins / Recombinant Proteins / Reverse Transcriptase Polymerase Chain Reaction / STAT3 Transcription Factor / シグナル伝達 (signal transduction) / Trans-Activators
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11437212
- ● Search Scopus @ Elsevier (PMID): 11437212
(PubMed: 11437212) H Yamada, F Nishimura, K Furuno, Koji Naruishi, Y Kobayashi, S Takashiba and Y Murayama :
Serum phenytoin concentration and IgG antibody titre to periodontal bacteria in patients with phenytoin-induced gingival overgrowth.,
Journal of the International Academy of Periodontology, Vol.3, No.2, 42-47, 2001.- (要約)
- Epileptic patients taking phenytoin with gingival-overgrowth and those without gingival-overgrowth were compared for daily drug dose, plasma total phenytoin concentration, plasma free-phenytoin concentration and serum IgG antibody titre against 13 periodontal bacteria. Significantly higher daily drug dose was noted in patients with gingival overgrowth (P < 0.05) when compared with those without overgrowth. In addition, both total and free forms of plasma phenytoin concentration were significantly higher in sera of patients with gingival growth than of those without overgrowth (P < 0.01). Strong positive correlation was found between daily drug dose and serum phenytoin concentration in patients with gingival overgrowth, while weak correlation was found in patients without gingival overgrowth, suggesting a difference in drug metabolism in these two groups. However, no differences were found in serum IgG antibody titres to 13 periodontal bacteria examined between two groups. These results suggest that metabolic ability of phenytoin is one of the factors for developing gingival overgrowth, and that periodontal infection may not be a primary causative factor for gingival overgrowth but act as an additive factor which increase tissue mass for this unwanted side effect.
- (キーワード)
- Administration, Oral / Adolescent / Adult / Aged / Aggregatibacter actinomycetemcomitans / Antibodies, Bacterial / Anticonvulsants / Bacteroides / Campylobacter / Capnocytophaga / Eikenella corrodens / Epilepsy / Female / Fusobacterium nucleatum / Gingival Overgrowth / Gram-Negative Bacteria / Humans / Immunoglobulin G / Male / Middle Aged / Phenytoin / Porphyromonas gingivalis / Prevotella intermedia / Risk Factors / Statistics as Topic / Treponema
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12666977
- ● Search Scopus @ Elsevier (PMID): 12666977
(PubMed: 12666977) H Ohe, S Takashiba, Koji Naruishi, H H Chou, H Yamada, F Nishimura, H Arai and Y Murayama :
Tumor necrosis factor-alpha (TNF-alpha)-induced and interleukin-1 beta (IL-1 beta)-induced shedding of TNF receptors from gingival fibroblasts.,
Journal of Interferon and Cytokine Research, Vol.20, No.12, 1077-1082, 2000.- (要約)
- Tumor necrosis factor-alpha (TNF-alpha) exerts its functions by binding two different receptors (TNFR55 and TNFR75). Both TNFR55 and TNFR75 exist in cell-associated and soluble forms. Soluble TNF receptors (sTNFR), sTNFR55 and sTNFR75, are proteolytically shed upon inflammatory stimuli and then modulate various TNF-alpha bioactivities. As human gingival fibroblasts (HGF) can be potential targets for TNF-alpha in inflamed gingiva, we hypothesized that HGF partially modulate the cellular responses to TNF-alpha by regulating their own TNFR. In this study, the kinetics of expression of cell-associated and soluble forms of both receptors from cultured HGF in response to proinflammatory cytokines TNF-alpha and interleukin-1 beta (IL-1 beta) were investigated in vitro. Both TNF-alpha and IL-1 beta upregulated the gene expression of TNFR75 and did not affect that of TNFR55. TNF-alpha and IL-1 beta decreased binding of [(125)I]TNF-alpha to HGF. Moreover, TNF-alpha and IL-1 beta upregulated the release of sTNFR75 from HGF but not that of sTNFR55. These results suggest that HGF under inflammatory conditions may contribute to the inactivation of circulating TNF-alpha through the preferential induction and shedding of TNFR75.
- (キーワード)
- Antigens, CD / Binding, Competitive / Cells, Cultured / Fibroblasts / Gingiva / Humans / 免疫組織化学 (immunohistochemistry) / Interleukin-1 / Iodine Radioisotopes / Receptors, Tumor Necrosis Factor / Receptors, Tumor Necrosis Factor, Type I / Receptors, Tumor Necrosis Factor, Type II / Tumor Necrosis Factor-alpha
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1089/107999000750053744
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11152574
- ● Search Scopus @ Elsevier (PMID): 11152574
- ● Search Scopus @ Elsevier (DOI): 10.1089/107999000750053744
(DOI: 10.1089/107999000750053744, PubMed: 11152574) H H Chou, S Takashiba, H Maeda, Koji Naruishi, F Nishimura, H Arai, H Lu and Y Murayama :
Induction of intracellular interleukin-1 beta signals via type II interleukin-1 receptor in human gingival fibroblasts.,
Journal of Dental Research, Vol.79, No.9, 1683-1688, 2000.- (要約)
- The type II interleukin-1 receptor (IL-1RII) has been thought to be incapable of transducing signals to cells because of its short intracellular domain, while type I IL-1 receptor (IL-1RI) does transduce signals. Since over-expression of IL-1RII has been demonstrated to inhibit cytokine production in the fibroblastic cell line, it has been proposed to use IL-1RII to prevent IL-1-induced inflammation in connective tissue. In this study, trace amounts of IL-1RII mRNA expression were detected in human gingival fibroblasts (HGFs), which are affected by cytokines in inflammatory periodontal disease. Cloning of the cDNA encoding IL-1RII expressed in HGFs revealed 3 amino acid substitutions in the extracellular domain, when compared with the 408 residues predicted from human B-cells. Over-expression of IL-1RII on HGFs by gene transfer down-regulated the expression of IL-1 beta mRNA and IL-6 mRNA in response to IL-1 beta stimulation, while the expression of IL-8 mRNA was not affected. In the IL-1RII-transfected HGFs, phosphorylation of 25- and 74-kDa proteins was up-regulated upon IL-1 beta stimulation in the transfected HGFs. The phosphorylation of these proteins was suppressed by the addition of a neutralizing antibody against IL-1RII. These results suggest that the IL-1RII may regulate HGFs expression of cytokine mRNA upon IL-1 beta stimulation, possibly by altering the IL-1RI-dependent signals.
- (キーワード)
- Base Sequence / Cells, Cultured / DNA Primers / Fibroblasts / 遺伝子発現 (gene expression) / Gingiva / Humans / Interleukin-1 / Molecular Sequence Data / リン酸化 (phosphorylation) / RNA, Messenger / Radioligand Assay / Receptors, Interleukin-1 / Reverse Transcriptase Polymerase Chain Reaction / シグナル伝達 (signal transduction) / Up-Regulation
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11023264
- ● Search Scopus @ Elsevier (PMID): 11023264
(PubMed: 11023264) F Nishimura, Koji Naruishi, H Yamada, T Kono, S Takashiba and Y Murayama :
High glucose suppresses cathepsin activity in periodontal-ligament-derived fibroblastic cells.,
Journal of Dental Research, Vol.79, No.8, 1614-1617, 2000.- (要約)
- The accumulation of extracellular matrices and integrins by high glucose has been reported in relation to diabetic complications. We previously reported that PDL cells expressed a higher amount of VLA-5 when cultured in high-glucose (4500 mg/L) medium than those cultured in low-glucose (1100 mg/L) medium. In this study, we aimed to address (1) whether this effect was mediated by the transcriptional level of the gene or the degradative level of the protein, and (2) whether this effect was mediated by TGF-beta. The results indicated that the level of mRNA encoding alpha5 integrin did not change in PDL cells regardless of the concentration of glucose. Alternatively, high glucose suppressed cathepsin B+L activity. Additionally, the level of mRNA encoding TGF-beta was not affected by high glucose, nor did an anti-TGF-beta neutralizing antibody have an effect on the expression of beta5 gene or cathepsin activity. Therefore, the effects of high glucose appeared to be mediated by impaired protein degradation, but not by autocrine TGF-beta.
- (キーワード)
- Autocrine Communication / Cathepsins / Cell Adhesion / Cells, Cultured / Culture Media / Down-Regulation / Fibroblasts / グルコース (glucose) / Humans / Hyperglycemia / Periodontal Ligament / Receptors, Fibronectin / Statistics, Nonparametric / Transcription, Genetic / Transforming Growth Factor beta
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11023284
- ● Search Scopus @ Elsevier (PMID): 11023284
(PubMed: 11023284) Yoji Asahara, Fusanori Nishimura, Hisa Yamada, Koji Naruishi, Masatoshi Kataoka, Jun-ichi Kido, Toshihiko Nagata and Yoji Murayama :
Mast cells are not involved in the development of cyclosporin A-induced gingival hyperplasia: a study with mast cell-deficient mice,
Journal of Periodontology, Vol.71, No.7, 1117-1120, 2000.- (要約)
- A previous study suggested that mast cells (MC) are involved in the development of cyclosporin A-induced gingival hyperplasia, since an increased number of MC were observed in the tissue sections of enlarged gingiva. To determine the role of MC in gingival hyperplasia, an MC-deficient mouse model was used in the current study. MC-deficient mice (WBB6F1xW/Wv) and their littermates (+/+) were fed sucrose-containing diets supplemented with or without varying concentrations (300, 400, 500, 600 mg) of cyclosporin A/kg of diet. After 30 days, the mice were sacrificed and the degree of gingival hyperplasia was evaluated by the appearance of the gingiva. Tissue MC were stained with toluidine blue to confirm the presence or absence of MC in the enlarged gingiva. Both W/Wv and +/+ mice, when fed with 600 mg cyclosporin A/kg diet for 30 days, exhibited a similar degree of gingival hyperplasia, while other test mice or control mice did not. Toluidine blue staining of the tissue sections confirmed the presence of MC in the enlarged gingiva of the +/+ mice, but not the W/Wv mice. These results indicate that mast cells are not necessary in the development of cyclosporin A-induced gingival hyperplasia, and that the increased number of MC observed in the enlarged gingiva may be a secondary effect of gingival hyperplasia. We also conclude that a study of mice lacking certain molecules or cells would be quite useful in determining the molecules or cell types responsible for the pathogenesis of drug-induced gingival hyperplasia.
- (キーワード)
- Animals / Coloring Agents / Cyclosporine / Gingival Hyperplasia / Immunosuppressive Agents / Mast Cells / Mice / Mice, Mutant Strains / Specific Pathogen-Free Organisms / Tolonium Chloride
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1902/jop.2000.71.7.1117
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10960018
- ● Search Scopus @ Elsevier (PMID): 10960018
- ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2000.71.7.1117
(DOI: 10.1902/jop.2000.71.7.1117, PubMed: 10960018) H Yamada, F Nishimura, Koji Naruishi, H H Chou, S Takashiba, M G Albright, S Nares, M A Iacopino and Y Murayama :
Phenytoin and cyclosporin A suppress the expression of MMP-1, TIMP-1, and cathepsin L, but not cathepsin B in cultured gingival fibroblasts.,
Journal of Periodontology, Vol.71, No.6, 955-960, 2000.- (要約)
- The results indicate that, besides suggested effects of these drugs on gingival fibroblasts and/or on accumulated cells in the gingival tissues, extracellular matrix-degrading ability, particularly that by cathepsin L, is also suppressed by cyclosporin A and phenytoin in gingival fibroblasts, and that lysosomal enzyme plays an important role in the pathogenesis of drug-induced gingival hyperplasia.
- (キーワード)
- Anticonvulsants / Cathepsin B / Cathepsin L / Cathepsins / Cell Division / Cells, Cultured / Cyclosporine / Cysteine Endopeptidases / Cysteine Proteinase Inhibitors / Endopeptidases / Enzyme Inhibitors / Enzyme Precursors / 細胞外マトリックス (extracellular matrix) / Fibroblasts / Gene Expression Regulation, Enzymologic / Gingiva / Gingival Hyperplasia / Humans / Lysosomes / Matrix Metalloproteinase Inhibitors / Phenytoin / Time Factors / Tissue Inhibitor of Metalloproteinase-1
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1902/jop.2000.71.6.955
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10914799
- ● Search Scopus @ Elsevier (PMID): 10914799
- ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2000.71.6.955
(DOI: 10.1902/jop.2000.71.6.955, PubMed: 10914799) Koji Naruishi, S Takashiba, H H Chou, H Arai, F Nishimura and Y Murayama :
Role of soluble interleukin-6 receptor in inflamed gingiva for binding of interleukin-6 to gingival fibroblasts.,
Journal of Periodontal Research, Vol.34, No.6, 296-300, 1999.- (要約)
- Interleukin-6 (IL-6), frequently detected in periodontitis, is known to mediate important signals in the inflammatory cytokine network. Gingival fibroblasts (GF) secrete cytokines upon stimulation with inflammatory mediators. However, it is not clear if GF respond to IL-6. We examined the IL-6 receptor gene expression in GF. Furthermore, we tested whether GF are target cells for IL-6 by examination of binding of IL-6. GF were found to contain trace amounts of mRNA for IL-6 receptor (IL-6R), but had high levels of mRNA for 130-kDa glycoprotein (gp130), which is a signal transducer for IL-6/IL-6R complex. Based on this observation, we hypothesized that IL-6 could bind GF if exogenous soluble forms of IL-6R (sIL-6R) existed in the gingiva or culture condition. Thus, we investigated the existence of sIL-6R in gingiva using enzyme-linked immunosorbent assay and whether sIL-6R influenced the binding of IL-6 to GF in vitro. In inflamed gingiva, sIL-6R was detected and its concentration ranged from 150 to 700 pg/microgram protein. The sIL-6R enhanced the binding of IL-6 to GF in a dose-dependent manner. This enhancement was inhibited by an antibody against gp130, suggesting that the IL-6/sIL-6R complex bound to the fibroblasts via gp130. These data demonstrated that gingival fibroblasts can be target cells for IL-6 in the presence of appropriate amounts of sIL-6R. This situation may exist during inflammation in periodontal tissue.
- (キーワード)
- Adult / Biopsy / Cells, Cultured / Chronic Disease / Enzyme-Linked Immunosorbent Assay / Fibroblasts / Gingiva / Gingivitis / Humans / Interleukin-6 / 分子量 (molecular weight) / 歯周病 (periodontitis) / Polymerase Chain Reaction / RNA, Messenger / Radioligand Assay / Receptors, Interleukin-6 / Solubility
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10633884
- ● Search Scopus @ Elsevier (PMID): 10633884
(PubMed: 10633884) 成石 浩司 :
線維芽細胞におけるIL-6の刺激伝達,
岡山歯学会雑誌, Vol.17, No.4, 33-43, 1998年.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1570009751801382528
(CiNii: 1570009751801382528) - MISC
- 木戸 淳一, 板東 美香, 稲垣 裕司, 生田 貴久, 梶浦 由加里, 中島 由紀子, 坂本 英次郎, 美原(和田) 智恵, 二宮 雅美, 西川 泰史, Jung-Hwan Lew, 成石 浩司, 永田 俊彦 :
歯肉溝滲出液中のバイオマーカーを用いた歯周病診断,
Journal of Oral Health and Biosciences, Vol.29, No.1, 13-20, 2016年.- (要約)
- Periodontal diseases cause an inflammation and degradation of periodontal tissues and missing of teeth. The incidence rate of periodontal diseases is high in middle-aged and elderly people.A reasonable diagnosis of periodontal diseases is very important to keep teeth, however, conventional examinations of periodontal diseases is not necessarily exact and objective. Gingival crevicular fluid (GCF) is an exudate secreted from periodontal tissues and contains many components including proteolytic enzymes, inflammatory cytokines, blood-associated proteins, cellular and bacterial fragments. Because some proteins in GCF are related to inflammation, tissue degradation and bone metabolism, those proteins have been studying as a diagnostic marker of periodontal diseases. GCF is noninvasively collected using a sterile paper strip and biomarkers are determined using enzyme-linked immunosorbent assay (ELISA) and enzyme activity assay. We identified calprotectin, an inflammationrelated protein, in GCF and calprotectin level in GCF from periodontitis sites was significantly higher than that of healthy control. Calprotectin level in GCF was positively correlated to gingival index and other biomarkers and decreased by periodontal treatments. Resistin is an adipocytokine and its level increases in some inflammatory diseases. Resistin level in GCF from periodontitis sites was high compared to the level of healthy control samples. Procollagen type I C-terminal peptide (PICP) is a biomarker for bone metabolism and its level was high in GCF collected from periodontitis sites. These results suggested that calprotectin, resistin and PICP are useful biomarkers for periodontal diseases. On the other hand, we showed that glycated albumin (GA), a marker of diabetes mellitus (DM), was contained in GCF and GA level in GCF from DM patients was significantly higher than that of non-DM individuals. Components in GCF may be biomarkers of systemic diseases as well as periodontal diseases and their determination will be useful diagnostic examination of some diseases. Recently, we have been studying the determining system of GCF calprotectin, including microchip ELISA, surface plasmon resonance assay and immuno-chromatography assay. When GCF biomarkers are determined using the determining systems, we will simply, exactly and objectively diagnose periodontal diseases at our dental offices.
- (キーワード)
- 歯周病診断 / バイオマーカー / 歯肉溝滲出液
- (徳島大学機関リポジトリ)
- ● Metadata: 109875
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1050845763956844416
(徳島大学機関リポジトリ: 109875, CiNii: 1050845763956844416) 内藤 仁美, 工藤 値英子, 目黒 道生, 成石 浩司, 伊東 孝, 前田 博史, 高柴 正悟 :
ある侵襲性歯周炎患者の26年間における歯周病治療の経過 -血清IgG抗体価による歯周病原細菌感染度もモニタリング-,
日本歯周病学会誌, Vol.56, No.2, 217-226, 2014年. Osamu Murai, Daisuke Sasaki, Yoshinori Ando, Akira Fujimura, Hiromi Oikawa, Nagisa Suwa, Daisuke Watabe, Fumihiko Maeda, Kohki Endo, Takashi Yaegashi, Toshihide Akasaka and Koji Naruishi :
Improvement of pustulosis palmaris et plantaris by periodontal infection control in a patient with chronic periodontitis.,
Clinical Laboratory, Vol.58, No.3-4, 323-327, 2012.- (要約)
- Pustulosis palmaris et plantaris (PPP) is a chronic, inflammatory, autoimmune-type disease characterized by sterile pustules of skin. The skin inflammation is influenced by several factors such as drugs, sunlight, metabolic and psychogenic factors as well as metal allergy. Here, we report a rare case that intensive periodontal treatment might have contributed to the improvement of skin inflammation. Skin inflammation regressed 1 month after intensive periodontal treatment. Both CD4/CD8 ratio and % of B cells in the blood sample were slightly decreased corresponding to the improvement of periodontal inflammation. Infection control of periodontal lesions might be one of attractive therapeutic targets in management of PPP.
- (キーワード)
- B-Lymphocytes / C-Reactive Protein / CD4-CD8 Ratio / Chronic Periodontitis / Humans / Leukocyte Count / Male / Middle Aged / Psoriasis / 皮膚微小循環 (microcirculation of the skin)
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22582507
- ● Summary page in Scopus @ Elsevier: 2-s2.0-84859815086
(PubMed: 22582507, Elsevier: Scopus) 成石 浩司, 澤田 俊輔, 村井 治, 武田 泰典, 川村 貴史, 若林 香枝, 桑島 幸紀, 三浦 廣行, 國松 和司 :
根未完成脱落歯に対するアペキシフィケーションを目的とした歯髄処置の経過報告,
岩手医科大学歯学雑誌, Vol.36, No.1, 53-58, 2011年.- (要約)
- 水酸化カルシウム製剤は,根未完成歯のアペキシフィケーションに用いる薬剤である.我々は,8歳の男児が転倒時に顔面を殴打し,右側上顎中切歯が完全脱臼した症例を経験した.脱臼歯は早急に整復固定したものの失活歯となり,同時に歯肉腫脹も認めたため,根管治療(アペキシフィケーション)が必要と診断された.根管内の失活歯髄を除去した後,市販の水酸化カルシウム製剤を適応した後,症状は速やかに改善した.今後約2~3年の経過観察の後,最終根管充填処置を行う必要があると考えられる.
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390001204587691008
(CiNii: 1390001204587691008) 成石 浩司, 國松 和司 :
重度歯周病患者における歯周病原性細菌に対する血清IgG抗体価の変化:症例報告,
岩手医科大学歯学雑誌, Vol.35, No.3, 146-152, 2010年.- (要約)
- 慢性辺縁性歯周炎は複数種の口腔細菌の感染によって発症し,炎症性骨吸収によって結果的に歯を喪失する感染症である.口腔内には500種類以上の細菌種が存在すると言われ,1980年代以降,多くの歯科医師によって歯周病の細菌学的な検討が行われてきた.とくに歯周病原性細菌の感染によって,その歯周病原細菌に対する血清中のIgG抗体価の上昇をきたすことが知られている.血清IgG抗体価のレベルは歯周病原細菌の量と比例するので,歯周病治療によって細菌量が減少すると,次第にIgG抗体価のレベルも減少すると考えられている.我々は重度歯周病患者の治療に相応して,複数種の歯周病原性細菌に対する血清IgG抗体価が減少した事例を経験したので,本症例報告において,血清IgG抗体価検査が歯周病治療の有効なマーカーになり得ることを提唱する.
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390001204588206208
(CiNii: 1390001204588206208) 工藤 値英子, 河野 隆幸, 西村 英紀, 大山 秀樹, 明貝 文夫, 成石 浩司, 岩本 義博, 高橋 直樹, 曽我 賢彦, 新井 英雄, 村山 洋二, 高柴 正悟 :
歯周治療により炎症マーカーが改善したと考察された重度歯周炎を伴うリウマチ患者の症例報告,
日本歯科保存学雑誌, Vol.46, No.1, 110-117, 2003年.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1570854176746500608
(CiNii: 1570854176746500608) Koji Naruishi, Akiko Kunita, Toshihiko Nagata, Shogo Takashiba and Seiji Adachi :
Cut-off values of Functional Independence Measure scores for discharge destination.,
Geriatrics & Gerontology International, Vol.15, No.5, 670-671, 2015.- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1111/ggi.12430
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25899761
- ● Summary page in Scopus @ Elsevier: 2-s2.0-84928136495
(DOI: 10.1111/ggi.12430, PubMed: 25899761, Elsevier: Scopus)
- 総説・解説
- 成石 浩司 :
歯周病と慢性腎臓病,
診断と治療, Vol.110, No.9, 1155-1158, 2022年9月.- (キーワード)
- 慢性腎臓病 / 歯周病 / 菌血症 / 骨代謝異常 / マンセイ ジンゾウビョウ / シシュウビョウ / キンケツショウ / コツ タイシャ イジョウ
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1520856528143534208
(CiNii: 1520856528143534208) 坂本 英次郎, 廣島 佑香, 木戸 淳一, 西川 泰史, 成石 浩司, 木戸 理恵, 湯本 浩通 :
カルプロテクチンの歯周病病態における多様な役割と歯周病診断マーカーとしての可能性,
日本歯周病学会会誌, Vol.62, No.4, 193-199, 2020年12月.- (キーワード)
- カルプロテクチン / 抗菌ペプチド / 歯周病 / DAMPs / 歯周病診断マーカー
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.2329/perio.62.193
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1391975831222787968
- ● Search Scopus @ Elsevier (DOI): 10.2329/perio.62.193
(DOI: 10.2329/perio.62.193, CiNii: 1391975831222787968) 成石 浩司, 湯本 浩通 :
糖尿病と慢性腎疾患(CKD),
月刊糖尿病, Vol.11, No.4, 80-85, 2019年10月. Koji Naruishi and Toshihiko Nagata :
Biological effects of interleukin-6 on Gingival Fibroblasts: Cytokine regulation in periodontitis.,
Journal of Cellular Physiology, Vol.233, No.9, 6393-6400, Mar. 2018.- (要約)
- Periodontitis is a bacterial infectious disease, and many inflammatory cytokines regulate periodontitis pathophysiology through a crosstalk between tissue cells and immune cells. Interleukin (IL)-6 is an important cytokine involved in the regulation of host response to bacterial infection. Human Gingival Fibroblasts (HGFs) are the most abundant cells in gingival connective tissues. Various HGF responses to periodontal pathogens or inflammatory cytokines contribute to the development of periodontitis. Lipopolysaccharide derived from Porphyromonas gingivalis (Pg LPS) and IL-1 significantly increase IL-6 production in HGFs. However, IL-6 cannot function in HGFs without the soluble form of the IL-6 receptor (sIL-6R), because HGFs do not express sufficient cell surface IL-6R to bind appreciable levels of IL-6. Importantly, sIL-6R is essential for IL-6 signaling in HGFs, and the sIL-6R is produced by differentiated THP-1 cells treated with IL-6. Calprotectin, a heterodimer of S100A8 and S100A9, is released during inflammation and significantly induces IL-6 production in HGFs via toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-B) signals. Calprotectin also induces sIL-6R production in differentiated THP-1 cells. IL-6 induces vascular endothelial growth factor (VEGF), matrix-metalloproteinase-1 (MMP-1), and cathepsin L production in HGFs in the presence of sIL-6R. Taken together, calprotectin-induced IL-6 production in HGFs may cause periodontitis progression through a crosstalk of fibroblasts and macrophages. There are many reports that examine how cytokines are released from HGFs to cause beneficial or harmful effects in inflamed periodontal lesions. This review explores the pathophysiology of periodontitis by focusing IL-6-mediated crosstalk of HGFs and macrophages.
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1002/jcp.26521
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29574949
- ● Search Scopus @ Elsevier (PMID): 29574949
- ● Search Scopus @ Elsevier (DOI): 10.1002/jcp.26521
(DOI: 10.1002/jcp.26521, PubMed: 29574949) Koji Naruishi and Yasufumi Nishikawa :
Crosstalk of Gingival Fibroblasts and Macrophages in Inflammatory Cytokine Cascade: Potential Mechanisms of Periodontitis,
Journal of Cell Signaling, Vol.2, No.2, e149, Jun. 2017.- (出版サイトへのリンク)
- ● Publication site (DOI): 10.4172/2576-1471.1000149
- (文献検索サイトへのリンク)
- ● Search Scopus @ Elsevier (DOI): 10.4172/2576-1471.1000149
(DOI: 10.4172/2576-1471.1000149) 成石 浩司, 永田 俊彦 :
最新の知見から攻める!①歯周病と腎疾患はどう関係するの?,
デンタルハイジーン, Vol.36, No.3, 304-305, 2016年3月. 成石 浩司, 永田 俊彦 :
歯周病が生活習慣病に及ぼす影響,
臨床栄養, Vol.126, No.3, 262-267, 2015年3月. 大森 一弘, 工藤 値英子, 成石 浩司, 前田 博史, 高柴 正悟 :
基礎研究から歯科臨床へ:歯周病原細菌に対する血漿IgG抗体価検査の可能性,
日本歯周病学会会誌, Vol.55, No.1, 9-14, 2013年.- (キーワード)
- 血漿 / IgG抗体価 / 歯周医学 / 客観的検査値
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.2329/perio.55.9
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390001204415954688
- ● Search Scopus @ Elsevier (DOI): 10.2329/perio.55.9
(DOI: 10.2329/perio.55.9, CiNii: 1390001204415954688) C T Thompson, A S Tahir, L Li, M Watanabe, Koji Naruishi, G Yang, D Kadmon, J C Logothetis, P Troncoso, C Ren, A Goltsov and S Park :
The role of caveolin-1 in prostate cancer: clinical implications.,
Prostate Cancer and Prostatic Diseases, Vol.13, No.1, 6-11, Jul. 2009.- (要約)
- Caveolin-1 (cav-1) is reportedly overexpressed in prostate cancer cells and is associated with disease progression. Specific oncogenic activities of cav-1 associated with Akt activation also occur in prostate cancer. A membrane-associated protein, cav-1, is nonetheless secreted by prostate cancer cells; results of recent studies showed that secreted cav-1 can stimulate cell survival and angiogenic activities, defining a role for cav-1 in the prostate cancer microenvironment. Serum cav-1 levels were also higher in prostate cancer patients than in control men without prostate cancer, and the preoperative serum cav-1 concentration had prognostic potential in men undergoing radical prostatectomy. Secreted cav-1 is therefore a potential biomarker and therapeutic target for prostate cancer.
- (キーワード)
- Caveolin 1 / Disease Progression / Humans / Male / Neovascularization, Pathologic / Prognosis / Prostatic Neoplasms / Tumor Markers, Biological / Up-Regulation
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1038/pcan.2009.29
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19581923
- ● Search Scopus @ Elsevier (PMID): 19581923
- ● Search Scopus @ Elsevier (DOI): 10.1038/pcan.2009.29
(DOI: 10.1038/pcan.2009.29, PubMed: 19581923) 成石 浩司 :
線維芽細胞を中心とした歯周病・歯肉増殖症の病態形成に関する基礎的研究,
日本歯周病学会会誌, Vol.51, No.1, 7-18, 2009年3月.- (出版サイトへのリンク)
- ● Publication site (DOI): 10.2329/perio.51.007
- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390282679388505984
- ● Search Scopus @ Elsevier (DOI): 10.2329/perio.51.007
(DOI: 10.2329/perio.51.007, CiNii: 1390282679388505984) Shogo Takashiba and Koji Naruishi :
Gene polymorphisms in periodontal health and disease.,
Periodontology 2000, Vol.40, 94-106, 2006.- (キーワード)
- Cytokines / Genetic Testing / Humans / Periodontal Diseases / 歯周病 (periodontitis) / Periodontium / Polymorphism, Genetic / Polymorphism, Single Nucleotide / Receptors, Immunologic
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1111/j.1600-0757.2005.00142.x
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16398687
- ● Search Scopus @ Elsevier (PMID): 16398687
- ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0757.2005.00142.x
(DOI: 10.1111/j.1600-0757.2005.00142.x, PubMed: 16398687) Shogo Takashiba, Koji Naruishi and Yoji Murayama :
Perspective of cytokine regulation for periodontal treatment: fibroblast biology.,
Journal of Periodontology, Vol.74, No.1, 103-110, Jan. 2003.- (要約)
- Efforts to understand the pathogenesis of periodontal diseases have been underway for decades. Studies of immunological aspects in addition to the structural components of gingival fibroblasts showed that the fibroblasts actively participate in immune and inflammatory events in periodontal diseases. Future strategies for the prevention and treatment of periodontal diseases should biologically regulate fibroblast activities. These cells are surrounded by monocyte-derived proinflammatory cytokines such as interleukin-1 beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and lymphocyte-derived interleukin-6 (IL-6) in inflamed gingival tissue. Recent anti-cytokine therapy for inflammatory diseases including rheumatoid arthritis aimed to inhibit the binding of cytokines to targeted cells such as fibroblasts and condrocytes. IL-1beta and TNF-alpha are thought to be therapeutic targets because these cytokines are essential for the initiation of inflammatory immune reactions and are produced for prolonged periods in inflammatory diseases. IL-6 is also a target, because it is abundantly present in inflammatory lesions and activates fibroblasts in the presence of soluble IL-6 receptor. In addition, these cytokines accelerate gingival fibroblasts to produce collagenolytic enzymes, resulting in tissue destruction. Soluble receptors for IL-1beta and TNF-alpha are suggested to be candidates for therapeutic molecules, but soluble receptor for IL-6 is suggested to be a factor-stimulating fibroblast. This paper will review the utilization of soluble receptors specific to inflammatory cytokines which potentially stimulate fibroblasts to regulate biological events involved in the pathogenesis of periodontal diseases.
- (キーワード)
- Anti-Inflammatory Agents / 細胞生物学 (cell biology) / Cytokines / Fibroblasts / Gingiva / Gingivitis / Humans / Interleukin-1 / Interleukin-6 / Matrix Metalloproteinase Inhibitors / Periodontal Diseases / 歯周病 (periodontitis) / Receptors, Interleukin-1 / Receptors, Interleukin-6 / Receptors, Tumor Necrosis Factor / シグナル伝達 (signal transduction) / Tumor Necrosis Factor-alpha
- (出版サイトへのリンク)
- ● Publication site (DOI): 10.1902/jop.2003.74.1.103
- (文献検索サイトへのリンク)
- ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12593604
- ● Search Scopus @ Elsevier (PMID): 12593604
- ● Search Scopus @ Elsevier (DOI): 10.1902/jop.2003.74.1.103
(DOI: 10.1902/jop.2003.74.1.103, PubMed: 12593604) - 講演・発表
- Yasufumi Nishikawa, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto :
Diabetic high-glucose condition enhances calprotectin-induced inflammatory responses in gingival fibroblasts,
97th General Session & Exhibition of the International Association for Dental Research (Vancouver, Canada), Jun. 2019. Yuji Inagaki, Kohei Nonaka, Ryosuke Takagi, Yasufumi Nishikawa, Rie Kido, Eijiro Sakamoto, Koji Naruishi, Jun-ichi Kido and Hiromichi Yumoto :
Kanroin Extracts Prevent Alveolar Bone Resorption in Experimental Rat Periodontitis,
96th General Session & Exhibition of the International Association of Dental Research, Jul. 2018. Yuka Hiroshima, Eijiro Sakamoto, Kaori Abe, Kaya Yoshida, Koji Naruishi, Toshihiko Nagata, Yasuo Shinohara, Geczy Carolyn and Jun-ichi Kido :
Advanced Glycation End-Products Increase Calprotectin in Human Gingival Epithelial Cells,
The 95th General Session & Exhibition of the International Association for Dental Research (IADR), San Francisco, Mar. 2017. Eijiro Sakamoto, Yuji Inagaki, Jun-ichi Kido, Takagi Ryosuke, Koji Naruishi and Toshihiko Nagata :
AGE and Porphyromonas gingival is-LPS Increase Sclerostin Expression in Osteocytes,
International Association for Dental Research, Mar. 2017.- (キーワード)
- 歯周病 (periodontitis) / 糖尿病 (diabetes mellitus) / 骨ミネラル代謝 (bone and mineral metabolism)
High glucose enhances IL-6-induced protease production in gingival fibroblasts,
94th General Session & Exhibition, International Association for Dental Research, Seoul, Jun. 2016. Yasufumi Nishikawa, Koji Naruishi, Yukari Kajiura, Jung-Hwan Lew, Jun-ichi Kido and Toshihiko Nagata :
Calprotectin induced the expression of inflammation-related molecules in gingival fibroblasts,
94th General Session & Exhibition, International Association for Dental Research, Seoul, Jun. 2016. Yukari Kajiura, Koji Naruishi, Yukiko Nakajima, Yasufumi Nishikawa, Jung-Hwan Lew, Jun-ichi Kido and Toshihiko Nagata :
High glucose enhaces P. gingivalis-induced cytokine production in THP-1 monocytes,
94th General Session & Exhibition, International Association for Dental Research, Seoul, Jun. 2016. Syotaro Yoshioka, Yoshiteru Tada, Junichiro Satomi, Kenji Yagi, Koji Naruishi, Kazuyuki Kuwayama, Keiko Kitazato, Takeshi Miyamoto, Yasuhisa Kanematsu, Masafumi Harada, Toshihiko Nagata and Shinji Nagahiro :
Impact of Periodontal Disease and Bacteria on Intracranial Aneurysms,
International Stroke Conference 2016, Los Angeles, Feb. 2016. Masami Ninomiya, Keiji Oishi, Hashimoto Mari, Koji Naruishi, Yamanouchi Kouji, Fukumura Yoshiaki and Toshihiko Nagata :
A Cross-Sectional Study on the Severity of Periodontitis in Infective Endocarditis Patients,
11th Asian Pacific Society of Periodontology Meeting, Oct. 2015.- (キーワード)
- 感染性心内膜炎 / 歯周病 (periodontitis) / 骨吸収 / 血清抗体価 / 疫学 (epidemiology)
YKL-40 in gingival crevicular fluid from patients with periodontitis and diabetes.,
Euro Perio 2015, Jun. 2015. Koji Naruishi and Toshihiko Nagata :
HGFs-macrophage crosstalk: sIL-6R secretion in THP-1 macrophages,
62th Annual Meeting of Japanese Association for Dental Reserch Abstract, Dec. 2014. 木戸 淳一, 廣島 佑香, 木戸 理恵, 吉田 賀弥, 稲垣 裕司, 成石 浩司, 湯本 浩通 :
人工合成したβ-defensin 2によるPorphyromonas gingivalisの付着抑制およびリポソーム封入と口腔上皮細胞への送達,
四国歯学会第60回例会, 2022年6月. 木戸 淳一, 廣島 佑香, 木戸 理恵, 吉田 賀弥, 稲垣 裕司, 成石 浩司, 湯本 浩通 :
人工合成したbeta-defensin 2によるPorphyromonas gingivalisの付着抑制およびリポソーム封入と口腔上皮細胞への送達,
第65回春季日本歯周病学会学術大会, 2022年6月. 木戸 理恵, 坂本 英次郎, 廣島 佑香, 板東 美香, 木戸 淳一, 生田 貴久, 二宮 雅美, 稲垣 裕司, 西川 泰史, 友竹 偉則, 成石 浩司, 湯本 浩通 :
イムノクロマト法を用いたカルプロテクチン測定による歯周病およびインプラント疾患の診断,
四国歯学会第59回例会, 2022年3月. 西川 泰史, 成石 浩司, 二宮 雅美, 植村 勇太, 湯本 浩通 :
2次性咬合性外傷を有する広汎型重度慢性歯周炎患者に包括的歯周治療を行った一症例,
日本歯科保存学会2021年度秋季学術大会(第155回)プログラムおよび講演抄録集, 2021年10月.- (キーワード)
- 侵襲性歯周炎
人工合成したLopocalin 2はPorphyromonas gingivalisの口腔上皮細胞への付着を抑制する,
第64回秋季日本歯周病学会学術大会, 2021年10月. 成石 浩司 :
幸せな「人生の最終段階」を目指して,歯科医療が貢献できること,
日本歯科保存学雑誌, 27, 2021年6月. 木戸 淳一, 廣島 佑香, 木戸 理恵, 吉田 賀弥, 稲垣 裕司, 成石 浩司, 湯本 浩通 :
リポソームに封入したリポカリン2の口腔上皮細胞への送達,
第64回春季日本歯周病学会学術大会, 2021年5月. 生田 貴久, 二宮 雅美, 秋月 皆人, 植村 勇太, 成石 浩司, 湯本 浩通 :
PCRを用いたPorphyromonas gingivalis2型線毛迅速検出システムの有効性の検討,
第64回春季日本歯周病学会学術大会プログラムおよび演題抄録集, Vol.63, 24, 2021年5月.- (キーワード)
- PCR / Porphyromonas gingivalis
PCRを用いたPorphyromonas gingivalis迅速検出システムの有用性,
日本歯科保存学会第153回 2020年度秋季学術大会, 2020年11月.- (キーワード)
- 歯周病 (periodontitis) / Porphyromonas gingivalis / PCR / 臨床検査 (clinical laboratory testing)
無細胞蛋白質合成系を用いた抗菌ペプチドの合成とリポソーム封入,
日本歯科保存学会2020年度春季学術大会(第152回)(神戸), 2020年6月. 廣島 佑香, 木戸 淳一, 木戸 理恵, 吉田 賀弥, 稲垣 裕司, 成石 浩司, 湯本 浩通 :
オーラルケアへの応用に関連するリポソームのデリバリー法の検討,
第63回春季日本歯周病学会学術大会, 2020年5月. 木戸 理恵, 廣島 佑香, 生田 貴久, 稲垣 裕司, 板東 美香, 成石 浩司, 木戸 淳一, 湯本 浩通 :
最終糖化産物による口腔上皮細胞の Lipocalin2 発現誘導は好中球の遊走性とサイトカイン発現を 調節する,
第63回春季日本歯周病学会学術大会, 2020年5月. 植村 勇太, 二宮 雅美, 和田 明大, 木戸 理恵, 高木 亮輔, 野中 康平, 谷口 裕哉, 生田 貴久, 坂本 英次郎, 板東 美香, 稲垣 裕司, 成石 浩司, 木戸 淳一, 湯本 浩通 :
歯周病ならびに歯周組織再生療法に関する臨床研究について,
徳島県歯科医学大会・四国歯学会第56回例会, 2020年2月. 二宮 雅美, 生田 貴久, 成石 浩司, 湯本 浩通 :
重度慢性歯周炎を有する血液透析患者に対して包括的歯周治療を行った一症例,
日本歯科保存学会 2019年度秋季学術大会(第151回), 2019年11月.- (キーワード)
- 歯周炎 (periodontal disease) / 透析 (dialysis) / 歯周治療 / ペリオドンタルメディシン
ショウガオールはヒト歯肉線維芽細胞においてAGEs誘導性の酸化ストレスを抑制する,
第62回秋季日本歯周病学会学術大会 (北九州), 2019年10月. 廣島 佑香, 木戸 淳一, 木戸 理恵, 吉田 賀弥, 稲垣 裕司, 成石 浩司, 湯本 浩通 :
オーラルケアへの応用を目指した抗菌ペプチド合成とリポソーム封入,
第62回秋季日本歯周病学会学術大会, 2019年10月. 高木 亮輔, 坂本 英次郎, 稲垣 裕司, 成石 浩司, 木戸 淳一, 湯本 浩通 :
S100A9はMAPKおよびSTAT3経路を介して骨細胞におけるIL-6とRANKLの発現を調節する,
日本歯科保存学会 2019年度春季学術大会(第150回) (金沢), 2019年6月. 二宮 雅美, 坂本 英次郎, 成石 浩司, 生田 貴久, 高木 亮輔, 畑中 加珠, 岡本 憲太郎, 小野 晋太郎, 高柴 正悟, 湯本 浩通 :
周期性好中球減少症を有する母娘に認められた重度歯周炎の症例,
日本歯周病学会会誌, Vol.61, 164, 2019年5月.- (キーワード)
- 周期性好中球減少症 / 家族性 / 重度歯周炎
最終糖化産物はヒト口腔上皮細胞のリポカリン2発現を増加する,
第62回春季日本歯周病学会学術大会, 2019年5月. 稲垣 裕司, 高木 亮輔, 西川 泰史, 木戸 理恵, 坂本 英次郎, 成石 浩司, 木戸 淳一, 湯本 浩通 :
甘露飲エキスは破骨細胞と骨芽細胞の分化制御を介してラット実験的歯周炎の歯槽骨吸収を抑制する,
日本歯科保存学会2018年度秋季学術大会(第149回), 2018年11月. 二宮 雅美, 生田 貴久, 成石 浩司, 湯本 浩通 :
口腔内細菌が原因で発症した感染性心内膜炎患者に対して包括的歯周治療を行った一症例,
日本歯科保存学会2018年度秋季学術大会(第149回), 163, 2018年11月.- (キーワード)
- 感染性心内膜炎 / 口腔内球菌 / 歯周治療
ショーガオールはヒト歯肉線維芽細胞におけるAGEs誘導性のIL-6およびICAM-1産生を抑制する,
第62回秋季日本歯周病学会学術大会, 2018年10月. 里見 淳一郎, 吉岡 正太郎, 宮本 健志, 成石 浩司, 北里 慶子, 多田 恵曜, 原田 雅史, 髙木 康志, 永廣 信治 :
脳動脈瘤と歯周病との関連,
日本脳神経外科学会第77回学術総会, 2018年10月. 西川 泰史, 成石 浩司, 木戸 淳一, 湯本 浩通 :
歯肉線維芽細胞におけるカルプロテクチン誘導性炎症関連因子の産生に及ぼす高グルコースの影響,
第148回日本歯科保存学会秋季学術大会, 2018年6月. 稲垣 裕司, 野中 康平, 高木 亮輔, 西川 泰史, 木戸 理恵, 坂本 英次郎, 成石 浩司, 木戸 淳一, 湯本 浩通 :
甘露飲エキス配合製剤はラット実験的歯周炎において歯槽骨吸収を抑制する,
第61回春季日本歯周病学会学術大会, 2018年6月. 野中 康平, 板東 美香, 木戸 淳一, 稲垣 裕司, 坂本 英次郎, 成石 浩司, 湯本 浩通 :
最終糖化産物はヒト歯肉線維芽細胞におけるIL-6とICAM-1の発現増加を介して単球との接着を誘導する,
第61回春季日本歯周病学会学術大会, 2018年6月. 木戸 理恵, 坂本 英次郎, 板東 美香, 稲垣 裕司, 二宮 雅美, 美原(和田) 智恵, 生田 貴久, 成石 浩司, 永田 俊彦, 木戸 淳一, 湯本 浩通 :
インプラント周囲溝滲出液中のカルプロテクチンとNTxを用いたインプラント疾患の診断,
第61回春季日本歯周病学会学術大会, 2018年6月. 高木 亮輔, 坂本 英次郎, 稲垣 裕司, 廣島 佑香, 成石 浩司, 木戸 淳一, 湯本 浩通 :
カルプロテクチンはマウス骨細胞の炎症および骨代謝関連因子の発現を制御する,
第61回春季日本歯周病学会学術大会, 2018年6月. 二宮 雅美, 稲垣 裕司, 美原(和田) 智恵, 板東 美香, 中島 由紀子, 坂本 英次郎, 生田 貴久, 西川 泰史, Jung-Hwan Lew, 木戸 理恵, 高木 亮輔, 野中 康平, 成石 浩司, 木戸 淳一, 永田 俊彦 :
新規歯周組織再生剤「リグロス歯科用液キット」の有効性,
四国歯学会 第51回例会, 2017年6月.- (キーワード)
- 歯周病 (periodontitis) / 塩基性線維芽細胞増殖因子 / 歯周組織再生療法 / リグロス
アドバンスドOSCEを見据えた当科の模擬OSCEの概要,
四国歯学会雑誌, Vol.29, No.2, 49-53, 2017年6月. 坂本 英次郎, 稲垣 裕司, 木戸 淳一, 高木 亮輔, 成石 浩司, 永田 俊彦 :
最終糖化産物とLPSはMAPKおよびNF-kBを介してマウス骨細胞のスクレロスチンの発現を調節する,
第60回春季日本歯周病学会学術大会, 2017年5月.- (キーワード)
- 歯周病 (periodontitis) / 糖尿病 (diabetes mellitus) / 骨ミネラル代謝 (bone and mineral metabolism) / 最終糖化産物 / リポ多糖
マウス骨細胞株MLO-Y4-A2のスクレロスチン発現における最終糖化産物およびLPSの影響,
第145回日本歯科保存学会秋季学術大会, 2016年10月. 板東 美香, 梶浦 由加里, 野中 康平, 坂本 英次郎, 成石 浩司, 木戸 淳一, 永田 俊彦 :
最終糖化産物はヒト歯肉線維芽細胞におけるIL-6およびICAM-1の発現を増加する,
第59回秋季日本歯周病学会学術大会, 2016年10月. 美原 智恵, 成石 浩司, 板東 美香, 西川 泰史, Jung-Hwan Lew, 坂本 英次郎, 生田 貴久, 河野 薫, 梶浦 由加里, 橋本 万里, 中島 由紀子, 稲垣 裕司, 二宮 雅美, 木戸 淳一, 永田 俊彦 :
アドバンスOSCEを見据えた当科の模擬OSCEの概要,
第49回四国歯学会例会, 2016年6月. 西川 泰史, 成石 浩司, 梶浦 由加里, Jung-Hwan Lew, 木戸 淳一, 永田 俊彦 :
カルプロテクチンはヒト歯肉線維芽細胞のTLR4を介して炎症性関連因子の発現を亢進する,
第144回日本歯科保存学会春季学術大会, 2016年6月. Jung-Hwan Lew, 成石 浩司, 梶浦 由加里, 西川 泰史, 木戸 淳一, 永田 俊彦 :
カロテノイドは高グルコース下で培養したヒト歯肉線維芽細胞のIL-6誘導性タンパク分解酵素産生を抑制する,
第59回春季日本歯周病学会学術大会, 2016年5月. 木戸 淳一, 板東 美香, 中島 由紀子, 梶浦 由加里, 稲垣 裕司, 生田 貴久, 坂本 英次郎, 成石 浩司, 永田 俊彦 :
ヒト口腔上皮細胞と歯肉線維芽細胞において低酸素環境が誘導する遺伝子発現の比較,
第143回日本歯科保存学会秋季学術大会, 2015年11月. 吉岡 正太郎, 多田 恵曜, 桑山 一行, 八木 謙次, 里見 淳一郎, 宮本 健志, 北里 慶子, 成石 浩司, 永田 俊彦, 原田 雅史, 永廣 信治 :
歯周病の重症度および原因菌は脳動脈瘤の発生と破裂に関与する,
一般社団法人 日本脳神経外科学会第74回学術総会, 2015年10月. 梶浦 由加里, 木戸 淳一, 中島 由紀子, 板東 美香, 稲垣 裕司, 成石 浩司, 坂本 英次郎, 阿部 佳織, 廣島 佑香, 永田 俊彦 :
低酸素環境が誘導するヒト口腔上皮細胞における遺伝子発現の解析,
第58回秋季日本歯周病学会学術大会, 2015年9月. 坂本 英次郎, 木戸 淳一, 梶浦 由加里, 板東 美香, 稲垣 裕司, 成石 浩司, 生田 貴久, 永田 俊彦 :
最終糖化産物はヒト口腔上皮細胞の遺伝子発現を調節する,
第58回秋季日本歯周病学会学術大会, 2015年9月. 成石 浩司, 梶浦 由加里, 西川 泰史, 板東 美香, 木戸 淳一, 永田 俊彦 :
培養歯肉線維芽細胞におけるクリプトタンシノンによる炎症関連分子の生産抑制効果,
第142回日本歯科保存学会春季学術大会, 2015年6月. 西川 泰史, 成石 浩司, 梶浦 由加里, 板東 美香, 木戸 淳一, 永田 俊彦 :
カルプロテクチンがヒト歯肉線維芽細胞の炎症関連因子の発現に及ぼす影響,
第58回春季日本歯周病学会学術大会, 2015年5月. 木戸 淳一, 永田 俊彦, 成石 浩司, 多部田 康一, 山崎 和久, 吉江 弘正, 渡邊 久, 和泉 雄一, 須田 玲子, 山本 松男, 柴 秀樹, 栗原 英見, 柳田 学, 北村 正博, 三島 昭宏, 水野 光春, 村上 伸也 :
イムノクロマト法を用いた歯肉溝滲出液中のカルプロテクチン測定による歯周病診断ー第2報ー,
第58回春季日本歯周病学会学術大会, 2015年5月. 二宮 雅美, 大石 慶二, 橋本 万里, 成石 浩司, 永田 俊彦 :
感染性心内膜炎発症患者における歯周病の進行度に関する横断的疫学調査,
日本歯科保存学会 2014年度秋季学術大会(第141回), 2014年10月.- (キーワード)
- 感染性心内膜炎 / 歯周病 (periodontitis) / 疫学 (epidemiology)
歯周病および糖尿病患者の歯肉溝滲出液中のYKL-40レベルの検討,
第57回秋季日本歯周病学会学術大会, 2014年10月. 成石 浩司 :
夜間ブラキシズムによる咬合性外傷によって進行した慢性歯周炎症例,
日本歯周病学会会誌, 2014年5月. 梶浦 由加里, 坂東 由記子, 木戸 淳一, 板東 美香, 稲垣 裕司, 中島 由紀子, 生田 貴久, 村田 裕美, 廣島 佑香, 成石 浩司, 永田 俊彦 :
歯周病および糖尿病患者の歯肉溝滲出液中のYKL-40レベルの検討,
第57回日本歯周病学会秋期学術大会抄録集, 2014年5月. 成石 浩司 :
歯周病の検査を考える(受賞講演II,岩手医科大学歯学会第73回例会抄録),
岩手医科大学歯学雑誌, Vol.37, No.1, 56, 2012年5月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390282679565750912
(CiNii: 1390282679565750912) 澤田 俊輔, 成石 浩司 :
高血糖状態で培養したヒト歯肉線維芽細胞の網羅的な遺伝子解析(一般演題,岩手医科大学歯学会第71回例会抄録),
岩手医科大学歯学雑誌, Vol.36, No.1, 80-81, 2011年5月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390001204587609600
(CiNii: 1390001204587609600) 成石 浩司 :
歯周疾患を標的とした臨床研究と細胞生物学的アプローチ(特別講演,岩手医科大学歯学会第70回例会抄録),
岩手医科大学歯学雑誌 = Dental journal of Iwate Medical University, Vol.35, No.2, 89, 2010年10月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1390282679564882688
(CiNii: 1390282679564882688) 園井 教裕, 前田 博史, 成石 浩司, 苔口 進, Amgad Wael HASSAN, 澤田 弘一, 小出 康史, 山部 こころ, 谷本 一郎, 新井 英雄, 高柴 正悟 :
Porphyromonas gingivalis の膿瘍形成能へ与えるnrdD様遺伝子の役割,
日本歯科保存学雑誌, Vol.51, 25, 2008年5月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1571698600650550144
(CiNii: 1571698600650550144) 冨山 高史, 成石 浩司, Rosalia MARTINEZ Zulema ARIAS, 山城 圭介, 前田 博史, 新井 英雄, 高柴 正悟 :
ラット根管治療モデルを用いた根尖周囲組織の遺伝子マイクロアレイ解析に基づいた根尖病巣治癒病態の考察,
日本歯科保存学雑誌, Vol.51, 141, 2008年5月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1571417125674114432
(CiNii: 1571417125674114432) Arias Zulema Rosalia MARTINEZ, 成石 浩司, 山城 圭介, 松浦 香織, 難波 尚子, 前田 博史, 新井 英雄, 高柴 正悟 :
ラット根管治療モデルを用いた根尖性歯周炎の治癒過程における網羅的な遺伝子解析,
日本歯科保存学雑誌, Vol.50, 155, 2007年5月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1571417125530187264
(CiNii: 1571417125530187264) 新井 英雄, 谷本 一郎, 岩本 義博, 小出 康史, 冨川 和哉, 冨山 高史, 下江 正幸, 園井 教裕, 成石 浩司, 高柴 正悟 :
歯周・歯内治療学の臨床教育に導入したe-ラーニングシステムの評価,
日本歯科保存学雑誌, Vol.49, 175, 2006年10月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1572543025406124928
(CiNii: 1572543025406124928) 山口 知子, 成石 浩司, 新井 英雄, 西村 英紀, 高柴 正悟 :
IL-6によるヒト歯肉線維芽細胞のリソソーム酵素カテプシンB, L活性の亢進における細胞膜蛋白カベオリン-1の関与,
日本歯周病学会会誌, Vol.48, 149, 2006年3月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1571698600304848000
(CiNii: 1571698600304848000) 山城 圭介, 成石 浩司, 山下 明子, 妹尾 京子, 山口 知子, 明貝 文夫, 新井 英雄, 西村 英紀, 高柴 正悟 :
高血糖状態で培養したヒト歯肉線維芽細胞の網羅的な遺伝子解析,
日本歯周病学会会誌, Vol.48, 197, 2006年3月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1573668925141840640
(CiNii: 1573668925141840640) 大森 一弘, 成石 浩司, 西村 英紀, 成石 比左, 山口 万有美, 新井 英雄, 高柴 正悟 :
高グルコース状態がヒト歯肉線維芽細胞のIL-6刺激伝達系に及ぼす影響 : gp130下流シグナル伝達経路の解明,
日本歯周病学会会誌, Vol.45, 139, 2003年9月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1572824499933812608
(CiNii: 1572824499933812608) 山口 万有美, 西村 英紀, 成石 浩司, 大森 一弘, 成石 比左, 高柴 正悟 :
サイクロスポリンの抗 angiogenic 効果はJNKの活性低下を介したVEGFの産生抑制による,
日本歯周病学会会誌, Vol.45, 140, 2003年9月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1573387449887227008
(CiNii: 1573387449887227008) 山口 万有美, 西村 英紀, 成石 比左, 曽我 賢彦, 苔口 進, 成石 浩司, 高柴 正悟 :
脂肪細胞は恒常的にTNF-αを産生し,その産生性は歯周病菌由来LPSによって亢進する,
日本歯周病学会会誌, Vol.45, 96, 2003年4月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1572261549739947520
(CiNii: 1572261549739947520) 大森 一弘, 成石 浩司, 西村 英紀, 成石 比左, 山口 万有美, 新井 英雄, 高柴 正悟 :
高グルコース状態は IL-6/sIL-6R 刺激によるヒト歯肉線維芽細胞の VEGF 産生を促進する,
日本歯科保存学雑誌, Vol.45, 60, 2002年10月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1574231875582015872
(CiNii: 1574231875582015872) 西村 英紀, 成石 比左, 成石 浩司, 高柴 正悟, 村山 洋二 :
B-22-15 : 40 カテプシン-L欠損マウスは歯肉増殖症を発症する,
日本歯周病学会会誌, Vol.44, No.0, 91, 2002年9月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1572261552229966848
(CiNii: 1572261552229966848) 山田 比左, 西村 英紀, 成石 浩司, 高柴 正悟, 村山 洋二 :
カルシウム拮抗剤ニフェジピンは歯肉線維芽細胞のカテプシンL活性を抑制する,
日本歯科保存学雑誌, Vol.44, 96, 2001年4月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1570572700175270400
(CiNii: 1570572700175270400) 成石 浩司, 高柴 正悟, 西村 英紀, 山田 比佐, 新井 英雄, 村山 洋二 :
C-24-15 : 40 ヒト歯肉線維芽細胞におけるリソソーム酵素カテプシンBおよびL活性へのIL-6刺激伝達系の関与,
日本歯周病学会会誌, Vol.43, No.0, 159, 2001年3月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1572824502183384832
(CiNii: 1572824502183384832) 山田 比左, 西村 英紀, 成石 浩司, 村山 洋二 :
抗てんかん薬フェニトインはヒト歯肉線維芽細胞のカテプシン活性を抑制する,
Tissue culture research communications : the journal of experimental & applied cell culture research = 組織培養研究, Vol.19, No.2, 91, 2000年6月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1570291225139890048
(CiNii: 1570291225139890048) 曽我 賢彦, 西村 英紀, 葛城 教子, 成石 浩司, 山田 比左, 佐藤 秀明, 高柴 正悟, 村山 洋二 :
β2-インテグリン発現異常を呈する早期発症型歯周炎患者,
日本歯科保存学雑誌, Vol.42, 77, 1999年10月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1573668924129506688
(CiNii: 1573668924129506688) 山田 比左, 西村 英紀, 成石 浩司, 小林 芳友, 高柴 正悟, 村山 洋二 :
フェニトイン服用患者における口腔病変,
日本歯科保存学雑誌, Vol.42, 203, 1999年10月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1572824499199206528
(CiNii: 1572824499199206528) 高柴 正悟, 大平 泰資, 明貝 文夫, 尾山 正高, 成石 浩司, 村山 洋二 :
歯髄組織の創傷治癒時に特徴的に発現する遺伝子,
日本歯科保存学雑誌, Vol.42, 17, 1999年4月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1573950399101801984
(CiNii: 1573950399101801984) 尾山 正高, 成石 浩司, 大平 泰資, 明貝 文夫, 高柴 正悟, 村山 洋二 :
歯髄細胞への外来遺伝子の導入に関する実験的研究,
日本歯科保存学雑誌, Vol.42, 18, 1999年4月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1572543024218249216
(CiNii: 1572543024218249216) 清水 明美, 西村 英紀, 成石 浩司, 澤田 聡子, 藤本 千代, 峯柴 淳二, 高柴 正悟, 村山 洋二 :
歯周病治療が誘因となって死亡したと疑われる症例,
日本歯周病学会会誌, Vol.41, No.1, 180, 1999年3月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1573387449152713600
(CiNii: 1573387449152713600) 大山 秀樹, 西村 英紀, 成石 浩司, 高柴 正悟, 村山 洋二 :
A-32-15 : 00 歯根膜線維芽細胞膜上のHLAクラスII分子の役割,
日本歯周病学会会誌, Vol.41, No.0, 89, 1999年3月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1572543027206796544
(CiNii: 1572543027206796544) 大江 丙午, 成石 浩司, 鷲尾 憲文, 新井 英雄, 西村 英紀, 高柴 正悟, 村山 洋二 :
B-18-14 : 20 炎症性サイトカインによるヒト歯肉線維芽細胞における可溶性TNF受容体の産生様態,
日本歯周病学会会誌, Vol.41, No.0, 107, 1999年3月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1573105977160214400
(CiNii: 1573105977160214400) 明貝 文夫, 太平 泰資, 山本 直史, 峯柴 淳二, 鷲尾 憲文, 成石 浩司, 新井 英雄, 西村 英紀, 高柴 正悟, 村山 洋二 :
B-13-11 : 10 ヒト歯根膜線維芽細胞が機械的刺激によって発現する特徴的な遺伝子の研究,
日本歯周病学会会誌, Vol.40, No.0, 108, 1998年9月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1574231877065372800
(CiNii: 1574231877065372800) 山田 比左, 西村 英紀, 成石 浩司, 高柴 正悟, 村山 洋二 :
B-17-14 : 00 シクロスポリンAおよびフェニトインは歯肉線維芽細胞の基質分解活性を抑制する,
日本歯周病学会会誌, Vol.40, No.0, 112, 1998年9月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1570291227391441280
(CiNii: 1570291227391441280) 大平 泰資, 明貝 文夫, 成石 浩司, 山本 直史, 新井 英雄, 西村 英紀, 高柴 正悟, 村山 洋二 :
ラット硬組織形成過程における糖質コルチコイド誘導性キナーゼ遺伝子(sgk)の発現パターン,
日本歯科保存学雑誌, Vol.41, 32, 1998年5月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1571698599292670208
(CiNii: 1571698599292670208) 成石 浩司, 高柴 正悟, 滝川 雅之, 西村 英紀, 新井 英雄, 村山 洋二 :
可溶性IL-6受容体を介する歯肉線維芽細胞のIL-6刺激伝達,
日本歯科保存学雑誌, Vol.40, 62, 1997年5月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1571980074264852608
(CiNii: 1571980074264852608) 大室 博正, 滝川 雅之, 岡村 和則, 西村 英紀, 成石 浩司, 澤 孝賢, 山本 直史, 大平 泰資, 高橋 慶壮, 郭 淑娟, 高柴 正悟, 村山 洋二 :
A Case Study of family Members Manifesting Early-Onset Periodontitis with Gingival Overgrowth ~Clinical, Microbiological, Immunological and Histological Observation~,
日本歯科保存学雑誌, Vol.40, 154, 1997年5月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1572543024217879296
(CiNii: 1572543024217879296) 成石 浩司, 新井 英雄, 高柴 正悟, 滝川 雅之, 鷲尾 憲文, 周 幸華, 大江 丙午, 浅原 洋士, 樋口 豊, 栗原 英見, 村山 洋二 :
A-34-10 : 50 ヒト歯肉線維芽細胞のIL-6刺激伝達における可溶性IL-6レセプターの役割,
日本歯周病学会会誌, Vol.37, No.0, 96, 1995年4月.- (文献検索サイトへのリンク)
- ● CiNii @ 国立情報学研究所 (CRID): 1573950402090200448
(CiNii: 1573950402090200448)
- 研究会・報告書
- 二宮 雅美, 坂本 英次郎, 成石 浩司, 湯本 浩通 :
周期性好中球減少症患者に発症した重度歯周炎の家族症例,
第1回侵襲性歯周炎センター クリニカルカンファレンス, 2018年12月.- (キーワード)
- 周期性好中球減少症 / 歯周炎 (periodontal disease) / 歯周治療
日本歯周病学会 ニュースレター 編集後記,
日本歯周病学会 ニュースレター, No.1, 18, 2020年4月.
- 特許
- 研究者総覧に該当データはありませんでした。
- 作品
- 研究者総覧に該当データはありませんでした。
- 補助金・競争的資金
- 老齢性テストステロン低下とAGE上昇に着目した糖尿病関連歯周炎の治療戦略 (研究課題/領域番号: 22K09965 )
糖尿病患者の歯周病重症化におけるIL-1作用と老齢性テストステロン低下の相乗効果 (研究課題/領域番号: 19K10131 )
人工細胞を用いたオーラルケアシステムの基礎研究 (研究課題/領域番号: 17H04418 )
糖尿病関連歯周炎のIL-6動態に着目したマクロファージ・線維芽細胞クロストーク (研究課題/領域番号: 16K11832 )
細胞性バイオマーカーを用いたインプラント疾患の診断とデバイス開発 (研究課題/領域番号: 15K15767 )
最終糖化産物とインフラマソームの関連から探る糖尿病関連歯周炎の病態 (研究課題/領域番号: 15K11391 )
最終糖化産物AGEsによる糖尿病関連歯周炎の重症化機序の解明と診断システムの構築 (研究課題/領域番号: 15H05054 )
AP-1によるカテプシン産生制御に着目した歯肉増殖症・歯周病診断の新機軸 (研究課題/領域番号: 24659926 )
前立腺癌の臓器転移に及ぼす歯周感染病巣の影響に関する基礎的研究 (研究課題/領域番号: 22592312 )
遷延する慢性感染が慢性閉塞性肺疾患の免疫応答に与える影響とその機序の解明 (研究課題/領域番号: 21590964 )
RhoAによる細胞分化機構を応用した歯根膜細胞移植治療のための基礎的研究 (研究課題/領域番号: 20592429 )
MMP-3を標的とした糖尿病患者における歯周病悪化メカニズムの分子生物学的解明 (研究課題/領域番号: 20592428 )
ラット根管治療モデルを用いたラミニンγ2発現動態からみた根尖病巣治癒メカニズム (研究課題/領域番号: 20592226 )
口腔ケアのための抗菌物質デリバリーシステムの開発 (研究課題/領域番号: 19592201 )
糖尿病患者の歯周病悪化を誘発する新規因子の網羅的な解析および同定 (研究課題/領域番号: 18791592 )
指尖毛細血管採血による血漿抗体価測定を用いた歯周病細菌感染度の判定法の研究 (研究課題/領域番号: 18209061 )
創傷歯髄から単離した新しい遺伝子FIP-2の象牙質・歯髄複合体形成への関わり (研究課題/領域番号: 17591991 )
末梢血幹細胞移植患者の口腔管理法確立のための基礎研究 (研究課題/領域番号: 13672186 )
研究者番号(00346446)による検索
- その他
- 研究者総覧に該当データはありませんでした。
2024年5月3日更新
- 専門分野・研究分野
- 歯周病学
歯内療法学 (Endodontology) - 所属学会・所属協会
- 日本歯周病学会
日本歯科薬物療法学会
日本口腔検査学会
日本歯科保存学会
日本臨床疫学会 - 委員歴・役員歴
- 日本歯周病学会 (編集委員 [2012年4月〜2015年3月])
日本歯周病学会 (広報委員会委員 [2019年4月〜2023年3月])
日本歯科薬物療法学会 ( [2011年1月〜2015年])
日本口腔検査学会 ( [2010年6月〜2015年])
日本歯科保存学会 ( [2004年2月〜2015年])
日本臨床疫学会 (第2回日本臨床疫学会査読委員 [2018年4月〜9月])
日本歯科保存学会 (評議員 [2017年4月〜2020年3月])
日本臨床疫学会 (第3回日本臨床疫学会査読委員 [2019年4月〜9月])
日本歯周病学会 (研究委員会委員 [2021年4月〜2023年3月])
日本歯周病学会 (日本歯周病学会奨励賞選考委員会委員 [2022年2月])
日本歯周病学会 (日本歯周病学会学術賞選考委員会委員 [2022年6月])
日本歯周病学会 (日本歯周病学会シーズ育成若手奨励研究助成選考委員会委員 [2021年9月]) - 受賞
- 2008年10月, 第8回日本歯周病学会学術賞 (日本歯周病学会)
2012年2月, 岩手医科大学歯学会雑誌 平成22年度優秀論文賞 (岩手医科大学歯学会) - 活動
- 徳島市 ( [2018年11月])
徳島大学 (新型コロナウイルス感染症にかかるワクチン職域接種 [2021年7月])
2024年4月28日更新
2024年5月4日更新
Jグローバル
- Jグローバル最終確認日
- 2024/5/4 01:05
- 氏名(漢字)
- 成石 浩司
- 氏名(フリガナ)
- ナルイシ コウジ
- 氏名(英字)
- Naruishi Koji
- 所属機関
- JグローバルAPIで取得できませんでした。
リサーチマップ
- researchmap最終確認日
- 2024/4/28 01:48
- 氏名(漢字)
- 成石 浩司
- 氏名(フリガナ)
- ナルイシ コウジ
- 氏名(英字)
- Naruishi Koji
- プロフィール
- リサーチマップAPIで取得できませんでした。
- 登録日時
- 2018/11/30 09:08
- 更新日時
- 2024/1/17 14:10
- アバター画像URI
- リサーチマップAPIで取得できませんでした。
- ハンドル
- リサーチマップAPIで取得できませんでした。
- eメール
- リサーチマップAPIで取得できませんでした。
- eメール(その他)
- リサーチマップAPIで取得できませんでした。
- 携帯メール
- リサーチマップAPIで取得できませんでした。
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- 学位
- 博士(歯学)
- 学位授与機関
- 岡山大学
- URL
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- 論文
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- リサーチマップAPIで取得できませんでした。
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- リサーチマップAPIで取得できませんでした。
2024年5月4日更新
- 研究者番号
- 00346446
- 所属(現在)
- 2024/4/1 : 徳島大学, 病院, 講師
- 所属(過去の研究課題
情報に基づく)*注記 - 2016/4/1 – 2022/4/1 : 徳島大学, 病院, 講師
2015/4/1 : 徳島大学, 大学病院, 講師
2012/4/1 : 岩手医科大学, 歯学部, 歯学部
2010/4/1 – 2012/4/1 : 岩手医科大学, 歯学部, 准教授
2010/4/1 : 岡山大学, 岡山大学病院, 講師
2010/4/1 : 岡山大学, 歯学部, 准教授
2009/4/1 : 岡山大学, 大学病院, 講師
2009/4/1 : 岩手大学, 歯学部, 准教授
2008/4/1 : 岡山大学, 医学部・歯学部附属病院, 講師
2008/4/1 : 岡山大学病院, 講師
2007/4/1 : 岡山大学, 大学院・医歯薬学総合研究科, 助教
2006/4/1 : 岡山大学, 大学院・医歯薬学総合研究科, 助手
2005/4/1 – 2006/4/1 : 岡山大学, 大学院医歯薬学総合研究科, 助手
2002/4/1 : 岡山大学, 歯学部附属病院, 助手
- 審査区分/研究分野
-
研究代表者
生物系 / 医歯薬学 / 歯学 / 歯周治療系歯学
小区分57030:保存治療系歯学関連研究代表者以外
生物系 / 医歯薬学 / 歯学 / 歯周治療系歯学
生物系 / 医歯薬学 / 歯学 / 保存治療系歯学
生物系 / 医歯薬学 / 内科系臨床医学 / 呼吸器内科学
医学 / 歯学 / 歯周治療系歯学
- キーワード
-
研究代表者
糖尿病 / 歯周病悪化メカニズム / 歯肉線維芽細胞 / 遺伝子マイクロアレイ解析 / MMP-3 / 歯周病悪化 / インターロイキン6 / マクロファージ / インターロイキン6レセプター / 糖尿病マウス / カテプシン / 歯周炎症 / プロテアーゼ / インターロイキン1 / gp130 / JNK / 糖尿病関連歯周炎 / 糖尿病性歯周炎 / 歯周病 / IL-6 / カルプロテクチン / 歯学 / 歯周病態 / テストステロン / IL-1 / 高齢者 / 超高齢者
研究代表者以外
慢性歯周炎 / 歯周病原細菌に対する血漿IgG抗体価 / 指尖採血 / 歯周病診断 / マルチセンター式研究 / 歯周病 / 歯周病菌に対するIgG抗体価 / 保存修復学 / 口腔感染症 / 口腔ケア / バイオフィルム / 感染症 / 根尖性歯周炎 / 骨芽細胞 / IL-1 / ラミニン / 病巣治癒 / インターロイキン1α / 根尖病巣 / 冶癒 / MAPK / インターロイキン1a / 細胞増殖活性 / 細胞接着活性 / 歯根膜 / 細胞分化 / RhoA-ROCKシグナル / Y-27632 / 遺伝子導入 / 遺伝子発現 / RhoA / ROCK / Rho / Rho-kinase / ストレスファイバー / COPD増悪 / 慢性感染 / 宿主免疫 / 感染 / 慢性閉塞性肺疾患 / 気道炎症 / 歯周炎 / 慢性炎症 / 癌転移 / がん転移 / 末梢血幹細胞移植 / 易感染性宿主 / 口腔管理 / 歯周疾患 / 細菌検査 / 白血球数 / PBSCT / compromised host / oral infection control / periodontal desease / bacterial detection / leukocyte / 象牙質・歯髄複合体 / ラット創傷歯髄 / TNF-αシグナル / プロモーター活性 / 転写因子結合部位 / 細胞死 / TNF-αパスウェイ / dentin-pulp complex / rat wounded pulp / TNF-α signaling / promoter activity / transcription factor-binding site / over-expression / cell death / 糖尿病関連歯周炎 / 最終糖化産物 / 歯肉線維芽細胞 / 炎症関連因子 / 炎症性サイトカイン / 酸化ストレス / インフラマソーム / インプラント疾患 / インプラント周囲溝液 / バイオマーカー / 診断デバイス / インプラント粘膜炎・周囲炎 / 疾患診断 / AGE / マクロファージ / 糖尿病性関連歯周炎 / 糖尿病 / オーラルケア / 抗菌ペプチド / 無細胞蛋白質合成 / リポソーム / ドラッグデリバリーシステム / 人工細胞 / 細菌付着抑制 / 無細胞蛋白合成