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福島圭穣

徳島大学

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2026年3月26日更新

職名: 准教授
電話: 研究者総覧に該当データはありませんでした。
電子メール: keijo.fukushima@tokushima-u.ac.jp
学歴: 2009/3: 静岡県立大学薬学部薬学科卒業
2011/3: 静岡県立大大学院薬学研究科博士前期課程修了
2014/9: 静岡県立大大学院薬学研究科博士後期課程修了
学位: 博士 / 博士(薬学) (静岡県立大学)
職歴・経歴: 2011/4: 本庄国際奨学金財団日本人大学院奨学生
2013/4: 日本学術振興会特別研究員(DC2)
2014/10: 静岡県立大学薬学部生化学分野客員共同研究員
2014/10: 日本学術振興会特別研究員(PD)
2015/4: 名古屋大学医学部附属病院薬剤部正規職員薬剤師
2017/4: 徳島大学大学院医歯薬学研究部生命薬学系分子情報薬理学分野助教

専門分野・研究分野: 研究者総覧に該当データはありませんでした。

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2026年3月26日更新

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担当経験のある授業科目: AI・Webツールアカデミー(AWA) (大学院)
健康生命薬学特論 (大学院)
創薬実践道場 (学部)
創薬研究実践特論 (大学院)
医療共用教育演習 (学部)
医薬品安全性学特論 (大学院)
学術論文作成法 (学部)
生物化学実習 (学部)
資源・環境共通演習 (大学院)
指導経験: 1人 (修士)

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2026年3月26日更新

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論文

Ayaka Hamaguchi, Hayato Fukuda, Mizuki Watanabe, Koichi Fujiwara, Keijo Fukushima, Satoshi Shuto and Hiromichi Fujino :
Resolvin E1 and Resolvin E2 suppress cyclooxygenase-2 expression through ubiquitin-proteasome-mediated degradation in human macrophage-like U937 cells.,
Prostaglandins & Other Lipid Mediators, 183, 2026.

(要約): Inflammatory responses comprise a crucial defense mechanism against infection and injury. Prostanoids, including prostaglandin E2 (PGE2), are well-known to play important roles in the generation of inflammatory responses. However, their excessive or prolonged activation can cause tissue damage and drive the development of diseases. Resolvin E-series (RvEs), including RvE1, RvE2, and RvE3, are specialized pro-resolving mediators that actively promote the resolution of inflammation. Here, using human macrophage-like U937 cells, we show that RvE1 and RvE2, but not RvE3, suppressed protein expression of cyclooxygenase (COX)-2, an essential and inducible enzyme involved in prostanoid synthesis during the onset of inflammatory responses. Furthermore, the suppression of COX-2 protein expression by RvE1 and RvE2 was suggested to involve enhanced ubiquitin-proteasome-dependent degradation, resulting in the rapid reduction of PGE2 production by decreasing functional COX-2. This is the first reported evidence that RvEs exert pro-resolving effects on macrophage-associated COX-2/PGE2 signaling. Importantly, RvEs reduced COX-2 expression at the low concentration of 10 nM without affecting COX-1 expression. Thus, they may represent promising candidates for novel anti-inflammatory drugs with potentially fewer gastrointestinal side effects than exhibited by many nonsteroidal anti-inflammatory drugs.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.prostaglandins.2026.107064
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 41707855; ● Search Scopus @ Elsevier (PMID): 41707855; ● Search Scopus @ Elsevier (DOI): 10.1016/j.prostaglandins.2026.107064

(DOI: 10.1016/j.prostaglandins.2026.107064, PubMed: 41707855) Hayato Fukuda, Kotaro Matsubara, Ayaka Hamaguchi, Hina Nishikoori, Mayu Shinohara, Jun Takouda, Kohsuke Takeda, Keijo Fukushima, Keita Komine, Koichi Fujiwara, Mizuki Watanabe, Jun Ishihara, Hiromichi Fujino and Satoshi Shuto :
Design and Synthesis of Cyclopropane Congeners of Resolvin E2 with Azidopropoxy Chain toward a Chemical Tool for Probing the Anti-inflammatory Activity.,
The Journal of Organic Chemistry, 91, 1, 466-476, 2025.

(要約): Resolvins (Rvs), unsaturated fatty acid metabolites are a new type of anti-inflammatory lipid mediator that promotes inflammation resolution, so that these compounds can be efficient leads for developing new anti-inflammatory drugs. We have previously developed a cyclopropane (CP) congener of resolving E2 (RvE2), i.e., CP-RvE2, as a stable equivalent of RvE2. In this study, based on the stable equivalent of CP-RvE2, we designed and synthesized AP-β-CP-RvE2, in which an azidopropoxy (AP) group was introduced into the 5-, 18-, or 20-position of CP-RvE2, as potential chemical probes. We found that among them, 5-AP-β-CP-RvE2 had anti-inflammatory activity same as RvE2, suggesting its potential utility as a chemical probe.
(キーワード): Cyclopropanes / Eicosapentaenoic Acid / Anti-Inflammatory Agents / 分子構造 (molecular structure) / Drug Design / Animals / Anti-Inflammatory Agents, Non-Steroidal / Mice / Azides / 構造活性相関 (structureactivity relationship)
(出版サイトへのリンク): ● Publication site (DOI): 10.1021/acs.joc.5c02534
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 41419324; ● Search Scopus @ Elsevier (PMID): 41419324; ● Search Scopus @ Elsevier (DOI): 10.1021/acs.joc.5c02534

(DOI: 10.1021/acs.joc.5c02534, PubMed: 41419324) Kanaho Senoo, Keijo Fukushima, Hitomi Yamamoto, Ayaka Hamaguchi, Akiko Suganami, Harumi Takano, Mayu Yamashita, W. John Regan, Yutaka Tamura and Hiromichi Fujino :
Potent activity of prostaglandin J2 on prostanoid DP receptors,
The Journal of Biological Chemistry, 301, 6, 108523, 2025.

(要約): Prostaglandin D₂ (PGD₂), an anti-inflammatory mediator, is acting through Gs-protein coupled D-type prostanoid (DP) receptors. DP receptors are not extensively distributed; in tissues, they are the least abundant among members of the prostanoid receptor family, whereas their primary ligand PGD₂ is the main prostanoid in most tissues. PGD₂ is dehydrated or isomerized to a number of metabolites enzymatically or nonenzymatically. To understand why many metabolites of PGD₂ are produced via different pathways, regular cell-based experiments, Black/Leff operational model calculations, and in silico simulations were utilized. Here we show that, among the five metabolites of PGD₂, prostaglandin J₂ (PGJ₂) was the most potent metabolite for DP receptors, particularly in the cAMP signaling pathway. This result was attributed to PGJ₂ forming an extra and/or stronger hydrogen bond by more negatively charged carbonyl in the cyclopentene ring with DP receptors than PGD₂. Therefore, when PGD₂ is released into the blood, it would activate DP receptors, which are then continuously activated by PGJ₂ to sustain the DP receptor/cAMP-mediated signaling pathway. Thus, the anti-inflammatory effects of PGD₂ may be taken over/out competed and/or even enhanced by PGJ₂. Here, PGJ₂ was found to be a standout mediator of cAMP-mediated signaling pathway, which induces more potent and prolonged DP receptor activities as a biased ligand, possibly for resolving the inflammatory reaction. Moreover, since each metabolite showed different properties, these results provide insight into why many metabolites of PGD₂ are produced and the miscellaneous physiological roles induced by the main prostanoid in most tissues through the least abundant DP receptors.
(キーワード): biased agonist / cAMP / DP prostanoid receptors / G-protein coupled receptors / operational model calculation / PGD2 / PGJ2 / prostaglandin / receptor regulation / β-catenin
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jbc.2025.108523
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 40254255; ● Summary page in Scopus @ Elsevier: 2-s2.0-105004925501

(DOI: 10.1016/j.jbc.2025.108523, PubMed: 40254255, Elsevier: Scopus) Haruka Okabayashi, Miki Yasuda, Chinatsu Nii, Ryo Sugishita, Keijo Fukushima, Kouki Yuasa, Satoshi Kotoura and Hiromichi Fujino :
Phosphatidylcholine-Plasmalogen-Oleic Acid Reduces BACE1 Expression in Human SH-SY5Y Cells.,
Biological & Pharmaceutical Bulletin, 47, 1, 192-195, 2024.

(要約): Plasmalogens are a family of glycerophospholipids containing one vinyl-ether bond at the sn-1 position in the glycerol backbone, and play important roles in cellular homeostasis including neural transmission. Therefore, reductions of plasmalogens have been associated with neurodegenerative disorders, such as Alzheimer's disease (AD). To evaluate the potential protective effects of plasmalogens against the pathology of AD, protein expression levels of key factors in amyloid precursor protein (APP) metabolic processes were examined using human neuroblastoma SH-SY5Y cells. Here, phosphatidylcholine-plasmalogen-oleic acid (PC-PLS-18) was shown to reduce protein expression levels of β-site APP cleaving enzyme 1 (BACE1), clusterin, and Tau, factors involved in the amyloid β-associated pathogenesis of AD. Thus, PC-PLS-18 may have preventive effects against AD by delaying the onset risk for a certain period.
(キーワード): Humans / Amyloid beta-Peptides / Amyloid Precursor Protein Secretases / Plasmalogens / Aspartic Acid Endopeptidases / Oleic Acid / Phosphatidylcholines / Neuroblastoma / Alzheimer Disease / Amyloid beta-Protein Precursor
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b23-00787
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38233149; ● Search Scopus @ Elsevier (PMID): 38233149; ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b23-00787

(DOI: 10.1248/bpb.b23-00787, PubMed: 38233149) Masaki Imanishi, Takahisa Inoue, Keijo Fukushima, Ryosuke Yamashita, Ryo Nakayama, Masataka Nojima, Kosuke Kondo, Yoshiki Gomi, Honoka Tsunematsu, Kohei Goto, Licht Miyamoto, Masafumi Funamoto, Masaya Denda, Keisuke Ishizawa, Akira Otaka, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya :
CA9 and PRELID2; hypoxia-responsive potential therapeutic targets for pancreatic ductal adenocarcinoma as per bioinformatics analyses.,
Journal of Pharmacological Sciences, 153, 4, 232-242, 2023.

(要約): A strong hypoxic environment has been observed in pancreatic ductal adenocarcinoma (PDAC) cells, which contributes to drug resistance, tumor progression, and metastasis. Therefore, we performed bioinformatics analyses to investigate potential targets for the treatment of PDAC. To identify potential genes as effective PDAC treatment targets, we selected all genes whose expression level was related to worse overall survival (OS) in The Cancer Genome Atlas (TCGA) database and selected only the genes that matched with the genes upregulated due to hypoxia in pancreatic cancer cells in the dataset obtained from the Gene Expression Omnibus (GEO) database. Although the extracted 107 hypoxia-responsive genes included the genes that were slightly enriched in angiogenic factors, TCGA data analysis revealed that the expression level of endothelial cell (EC) markers did not affect OS. Finally, we selected CA9 and PRELID2 as potential targets for PDAC treatment and elucidated that a CA9 inhibitor, U-104, suppressed pancreatic cancer cell growth more effectively than 5-fluorouracil (5-FU) and PRELID2 siRNA treatment suppressed the cell growth stronger than CA9 siRNA treatment. Thus, we elucidated that specific inhibition of PRELID2 as well as CA9, extracted via exhaustive bioinformatic analyses of clinical datasets, could be a more effective strategy for PDAC treatment.
(キーワード): Humans / Carbonic Anhydrase IX / Antigens, Neoplasm / Carcinoma, Pancreatic Ductal / Pancreatic Neoplasms / Hypoxia / RNA, Small Interfering / Computational Biology / Pancreatic Neoplasms
(徳島大学機関リポジトリ): ● Metadata: 2011889
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jphs.2023.10.003
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37973221; ● CiNii @ 国立情報学研究所 (CRID): 1050022708917887616; ● Search Scopus @ Elsevier (PMID): 37973221; ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2023.10.003

(徳島大学機関リポジトリ: 2011889, DOI: 10.1016/j.jphs.2023.10.003, PubMed: 37973221, CiNii: 1050022708917887616) Ayaka Hamaguchi, Hayato Fukuda, Koichi Fujiwara, Tomofumi Harada, Keijo Fukushima, Satoshi Shuto and Hiromichi Fujino :
Individual resolvin E family members work distinctly and in a coordinated manner in the resolution of inflammation.,
Prostaglandins & Other Lipid Mediators, 168, 106759, 2023.

(要約): Three main E-type resolvins (RvEs): RvE1, RvE2, and RvE3, have roles in the resolution of inflammation as anti-inflammatory activities. To investigate the roles of each RvE in the resolution of inflammation, timing of interleukin (IL)- 10 release and IL-10 receptor expressions, and phagocytosis evoked by each RvE in differentiated human monocytes, macrophage-like U937 cells were examined. Here, we show that RvEs enhance the expression of IL-10, and IL-10 receptor-mediated signaling pathways and IL-10-mediated-signaling-independent resolution of inflammatory effects by activating the phagocytotic function. Thus, RvE2 mainly evoked an IL-10-mediated anti-inflammatory function, whereas RvE3 principally activated phagocytotic activity of macrophages, which may be involved in tissue repair. On the other hand, RvE1 showed both functions, although not prominent but rather acting as a relief mediator that takes over the RvE2 function and passes over to the RvE3 function. Therefore, each RvE may act as an important role/stage-specific mediator in a coordinated manner with other RvEs in the processes of the resolution of inflammation.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.prostaglandins.2023.106759
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37327943; ● Summary page in Scopus @ Elsevier: 2-s2.0-85163220563

(DOI: 10.1016/j.prostaglandins.2023.106759, PubMed: 37327943, Elsevier: Scopus) Yuya Horinouchi, Yuka Murashima, Yuto Yamada, Shun Yoshioka, Keijo Fukushima, Takumi Kure, Naofumi Sasaki, Masaki Imanishi, Hiromichi Fujino, Koichiro Tsuchiya, Kazuaki Shinomiya and Yasumasa Ikeda :
Pemafibrate inhibited renal dysfunction and fibrosis in a mouse model of adenine-induced chronic kidney disease.,
Life Sciences, 321, 121590, 2023.

(要約): The risks associated with conventional fibrates (fenofibrate, bezafibrate) to the kidneys were evaluated using the Food and Drug Administration Adverse Event Reporting System. Pemafibrate (1 or 0.3 mg/kg/day) was administered daily using an oral sonde. Its renoprotective effects were examined in unilateral ureteral obstruction (UUO)-induced renal fibrosis model mice (UUO mice) and adenine-induced CKD model mice (CKD mice).
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.lfs.2023.121590
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36940907; ● CiNii @ 国立情報学研究所 (CRID): 1360017282221457024; ● Summary page in Scopus @ Elsevier: 2-s2.0-85151399970

(DOI: 10.1016/j.lfs.2023.121590, PubMed: 36940907, CiNii: 1360017282221457024, Elsevier: Scopus) Takahiro Niimura, Yoshito Zamami, Koji Miyata, Takahisa Mikami, Mizuho Asada, Keijo Fukushima, Masaki Yoshino, Satoru Mitsuboshi, Naoto Okada, Hirofumi Hamano, Takumi Sakurada, Rie Matsuoka-Ando, Fuka Aizawa, Kenta Yagi, Mitsuhiro Goda, Masayuki Chuma, Toshihiro Koyama, Yuki Izawa-Ishizawa, Hiroaki Yanagawa, Hiromichi Fujino, Yoshihiro Yamanishi and Keisuke Ishizawa :
Characterization of Immune Checkpoint Inhibitor-Induced Myasthenia Gravis Using the US Food and Drug Administration Adverse Event Reporting System.,
Journal of Clinical Pharmacology, 63, 4, 473-479, 2022.

(要約): Myasthenia gravis (MG) is a rare but fatal adverse event of immune checkpoint inhibitors (ICIs). We assessed whether patient characteristics differed between those with ICI-related myasthenia gravis and those with idiopathic myasthenia gravis. Reports from the US Food and Drug Administration Adverse Event Reporting System were analyzed. Multivariate analyses were conducted to evaluate the associations between age, sex, and ICI treatment and the reporting rate of myasthenia gravis. Among 5 464 099 cases between 2011 and 2019, 53 447 were treated with ICIs. Myasthenia gravis was reported more often in ICI users. Multiple logistic regression analyses showed that the reporting rate of ICI-related myasthenia gravis did not differ significantly between men and women; however, it was higher in older people than in younger people (adjusted odds ratio, 2.4 [95%CI, 1.84-3.13]). We also investigated useful signs for the early detection of myositis and myocarditis, which are fatal when overlapping with ICI-related myasthenia gravis. Patients with elevated serum creatine kinase or troponin levels were more likely to have concurrent myositis and myocarditis. Unlike idiopathic myasthenia gravis, there was no sex difference in the development of ICI-related myasthenia gravis, which may be more common in older people. Considering the physiological muscle weakness that occurs in the elderly, it may be necessary to monitor ICI-related myasthenia gravis more closely in older people.
(キーワード): Male / United States / Humans / Female / Aged / Immune Checkpoint Inhibitors / United States Food and Drug Administration / Myocarditis / Myasthenia Gravis / Myositis
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/jcph.2187
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36453166; ● Search Scopus @ Elsevier (PMID): 36453166; ● Search Scopus @ Elsevier (DOI): 10.1002/jcph.2187

(DOI: 10.1002/jcph.2187, PubMed: 36453166) Natsuki Yamagiwa, Haruka Kobayashi, Haruka Okabayashi, Miki Yasuda, Keijo Fukushima, Jun Kawamura, Satoshi Kotoura and Hiromichi Fujino :
Phosphatidylcholine-Plasmalogen-Oleic Acid Has Protective Effects against Arachidonic Acid-Induced Cytotoxicity.,
Biological & Pharmaceutical Bulletin, 45, 5, 643-648, 2022.

(要約): Plasmalogens are a group of glycerophospholipids containing a vinyl-ether bond at the sn-1 position in the glycerol backbone. Cellular membrane plasmalogens are considered to have important roles in homeostasis as endogenous antioxidants, differentiation, and intracellular signal transduction pathways including neural transmission. Therefore, reduced levels of plasmalogens have been suggested to be associated with neurodegenerative diseases such as Alzheimer's disease. Interestingly, although arachidonic acid is considered to be involved in learning and memory, it could be liberated and excessively activate neuronal activity to the excitotoxic levels seen in Alzheimer's disease patients. Here, we examined the protective effects of several kinds of plasmalogens against cellular toxicity caused by arachidonic acid in human neuroblastoma SH-SY5Y cells. As a result, only phosphatidylcholine-plasmalogen-oleic acid (PC-PLS-18) showed protective effects against arachidonic acid-induced cytotoxicity based on the results of lactate dehydrogenase release and ATP depletion assays, as well as cellular morphological changes in SH-SY5Y cells. These results indicate that PC-PLS-18 protects against arachidonic acid-induced cytotoxicity, possibly via improving the stability of the cellular membrane in SH-SY5Y cells.
(キーワード): Alzheimer Disease / Arachidonic Acid / Humans / Lecithins / Oleic Acid / Plasmalogens
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b22-00035
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35236811; ● Search Scopus @ Elsevier (PMID): 35236811; ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b22-00035

(DOI: 10.1248/bpb.b22-00035, PubMed: 35236811) Yoshito Zamami, Takahiro Niimura, Takehiro Kawashiri, Mitsuhiro Goda, Yutaro Naito, Keijo Fukushima, Soichiro Ushio, Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Kenta Yagi, Koji Miyata, Kenshi Takechi, Masayuki Chuma, Toshihiro Koyama, Daisuke Kobayashi, Takao Shimazoe, Hiromichi Fujino, Yuki Izawa-Ishizawa and Keisuke Ishizawa :
Identification of prophylactic drugs for oxaliplatin-induced peripheral neuropathy using big data.,
Biomedicine & Pharmacotherapy, 148, 2022.

(要約): Thus, drug repositioning using data from large-scale basic and clinical databases enables the discovery of new indications for approved drugs with a high probability of success.
(キーワード): Animals / Anticholesteremic Agents / Antineoplastic Agents / Big Data / Databases, Factual / Drug Repositioning / Humans / Hyperalgesia / Japan / Male / Mice / Mice, Inbred BALB C / Oxaliplatin / Peripheral Nervous System Diseases / Pre-Exposure Prophylaxis / Rats / Rats, Sprague-Dawley / Retrospective Studies / Simvastatin
(徳島大学機関リポジトリ): ● Metadata: 2010230
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.biopha.2022.112744
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35240525; ● Search Scopus @ Elsevier (PMID): 35240525; ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2022.112744

(徳島大学機関リポジトリ: 2010230, DOI: 10.1016/j.biopha.2022.112744, PubMed: 35240525) Kana Kitagawa, Ayaka Hamaguchi, Keijo Fukushima, Yuki Nakano, W John Regan, Masato Mashimo and Hiromichi Fujino :
Interleukin-4 may suppress expression of E-type prostanoid receptor4 in human colorectal cancer HCA-7 cells,
European Journal of Pharmacology, 920, 2022.

(要約): in the human colon cancer cell line, HCA-7. This result may be attributed to a reduction in the expression of prostanoid EP4 receptors through the induction of hypoxia inducible factor-1α via the interleukin-4 receptor-stimulated activation of signal transducer and activator of transcription 6. However, another major Th2 cytokine IL-13 had no effect on the expression of COX-2 or prostanoid EP4 receptors in HCA-7 cells. Therefore, instead of the hyperactivation of Th1/Th17 cells, the deactivation/down-regulation of Th2 cells followed by a decrease in the production of IL-4 in IBD may play a role in the cancerous transformation of cells, at least in prostanoid EP4 receptor-overactivated tumorigenesis.
(キーワード): Colonic Neoplasms / Cyclooxygenase 2 / Dinoprostone / Down-Regulation / Humans / Interleukin-4 / Prostaglandins E / Receptors, Prostaglandin E, EP2 Subtype / Receptors, Prostaglandin E, EP4 Subtype
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ejphar.2022.174863
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35240193; ● Search Scopus @ Elsevier (PMID): 35240193; ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2022.174863

(DOI: 10.1016/j.ejphar.2022.174863, PubMed: 35240193) Keijo Fukushima, Kanaho Senoo, Naoki Kurata, W John Regan and Hiromichi Fujino :
The Gαs-protein-mediated pathway may be steadily stimulated by prostanoid EP2 receptors, but not by EP4 receptors.,
FEBS Open Bio, 12, 4, 775-783, 2022.

(要約): causes accumulation of cAMP in EP2 receptors, whereas markedly low levels of cAMP accumulated in EP4 receptors. By applying the Black/Leff operational model calculation, we found that EP2 receptors have a biased ability to intrinsically activate the Gαs-protein-mediated pathway, whereas EP4 receptors have strong biased activity for the Gαi-protein-mediated pathway. Thus, EP2 and EP4 receptors may not be similar Gαs-coupled receptors but instead substantially different receptors with distinct roles.
(キーワード): Prostaglandins / Receptors, Prostaglandin E, EP2 Subtype / Receptors, Prostaglandin E, EP4 Subtype / Signal Transduction
(徳島大学機関リポジトリ): ● Metadata: 2010258
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/2211-5463.13378
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35124898; ● Search Scopus @ Elsevier (PMID): 35124898; ● Search Scopus @ Elsevier (DOI): 10.1002/2211-5463.13378

(徳島大学機関リポジトリ: 2010258, DOI: 10.1002/2211-5463.13378, PubMed: 35124898) Keijo Fukushima and Hiromichi Fujino :
Identification and Characterization of Human Colorectal Cancer Cluster Predominantly Expressing EP3 Prostanoid Receptor Subtype.,
Biological & Pharmaceutical Bulletin, 45, 6, 698-702, 2022.

(要約): ) is a well-known mediator of colorectal cancer through stimulation of four E-type prostanoid (EP) receptor subtypes: EP1, EP2, EP3, and EP4 receptors. All subtypes of EP receptors are involved in CRC promotion or malignancy. However, the characteristics of CRC that highly expresses EP receptor subtypes have not been clarified. In the present study, we classified CRC from a cancer genomic database and identified CRC clusters which highly express EP receptor subtypes. Most of these clusters predominantly expressed one subtype of EP receptor and showed different gene expression patterns. Among them, we focused on the cluster highly expressing the EP3 receptor (CL-EP3). As the result of characterization of gene expression, CL-EP3 was characterized as: epithelial mesenchymal transition (EMT)-induced progressed cancer with activation of transforming growth factor-β pathway, activation of hypoxia-inducible factor-1α, and suppression of runt-related transcription factor 3. Since we previously reported that EP3 receptor is involved in and induce colon cancer cell migration, EP3 receptor-expressing CRC may induce metastasis through these signaling pathways. Thus, the findings suggest the effectiveness of cancer clustering by gene expression of the EP receptor subtype to elucidate the mechanism of human CRC.
(キーワード): Colorectal Neoplasms / Dinoprostone / Humans / Receptors, Prostaglandin E / Signal Transduction
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b22-00104
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35650098; ● CiNii @ 国立情報学研究所 (CRID): 1390292251338536320; ● Summary page in Scopus @ Elsevier: 2-s2.0-85131270255

(DOI: 10.1248/bpb.b22-00104, PubMed: 35650098, CiNii: 1390292251338536320, Elsevier: Scopus) Hirofumi Hamano, Yasumasa Ikeda, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Masayuki Chuma, Michiko Yamashita, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Izawa-Ishizawa Yuki, Licht Miyamoto, Ishizawa Keisuke, Hiromichi Fujino, Toshiaki Tamaki, Ken-ichi Aihara and Koichiro Tsuchiya :
Diphenhydramine may be a preventive medicine against cisplatin-induced kidney toxicity,
Kidney International, 99, 4, 885-889, 2021.

(要約): Cisplatin is widely used as an anti-tumor drug for the treatment of solid tumors. Unfortunately, it causes kidney toxicity as a critical side effect, limiting its use, given that no preventive drug against cisplatin-induced kidney toxicity is currently available. Here, based on a repositioning analysis of the Food and Drug Administration Adverse Events Reporting System, we found that a previously developed drug, diphenhydramine, may provide a novel treatment for cisplatin-induced kidney toxicity. To confirm this, the actual efficacy of diphenhydramine was evaluated in in vitro and in vivo experiments. Diphenhydramine inhibited cisplatin-induced cell death in kidney proximal tubular cells. Mice administered cisplatin developed kidney injury with significant dysfunction (mean plasma creatinine: 0.43 vs 0.15 mg/dl) and showed augmented oxidative stress, increased apoptosis, elevated inflammatory cytokines, and MAPKs activation. However, most of these symptoms were suppressed by treatment with diphenhydramine. Furthermore, the concentration of cisplatin in the kidney was significantly attenuated in diphenhydramine-treated mice (mean platinum content: 70.0 vs 53.4 μg/g dry kidney weight). Importantly, diphenhydramine did not influence or interfere with the anti-tumor effect of cisplatin in any of the in vitro or in vivo experiments. In a selected cohort of 98 1:1 matched patients from a retrospective database of 1467 patients showed that patients with malignant cancer who had used diphenhydramine before cisplatin treatment exhibited significantly less acute kidney injury compared to ones who did not (6.1 % vs 22.4 %, respectively). Thus, diphenhydramine demonstrated efficacy as a novel preventive medicine against cisplatin-induced kidney toxicity.
(徳島大学機関リポジトリ): ● Metadata: 2008329
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.kint.2020.10.041
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33307103; ● Search Scopus @ Elsevier (PMID): 33307103; ● Search Scopus @ Elsevier (DOI): 10.1016/j.kint.2020.10.041

(徳島大学機関リポジトリ: 2008329, DOI: 10.1016/j.kint.2020.10.041, PubMed: 33307103) Iori Okura, Nanae Hasuoka, Kanaho Senoo, Akiko Suganami, Keijo Fukushima, W John Regan, Masato Mashimo, Toshihiko Murayama, Yutaka Tamura and Hiromichi Fujino :
The differential functional coupling of phosphodiesterase 4 to human DP and EP2 prostanoid receptors stimulated with PGD 2 or PGE 2,
Pharmacological Reports : PR, 73, 3, 946-953, 2021.

(キーワード): Adenylyl Cyclases / Cell Line / Cyclic AMP / Cyclic Nucleotide Phosphodiesterases, Type 4 / Dinoprostone / HEK293 Cells / Humans / Ligands / Prostaglandin D2 / Receptors, Immunologic / Receptors, Prostaglandin / Receptors, Prostaglandin E, EP2 Subtype / Signal Transduction
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s43440-021-00247-x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33786738; ● Search Scopus @ Elsevier (PMID): 33786738; ● Search Scopus @ Elsevier (DOI): 10.1007/s43440-021-00247-x

(DOI: 10.1007/s43440-021-00247-x, PubMed: 33786738) Motofumi Suzuki, Atsumi Urabe, Sayaka Sasaki, Ryo Tsugawa, Satoshi Nishio, Haruka Mukaiyama, Yoshiko Murata, Hiroshi Masuda, M. Sann Aung, Akane Mera, Masaki Takeuchi, Keijo Fukushima, Michika Kanaki, Kaori Kobayashi, Yudai Chiba, Binod Babu Shrestha, Hiromi Nakanishi, T. Watanabe, Atsushi Nakayama, Hiromichi Fujino, Takanori Kobayashi, Keiji Tanino, Naoko Nishizawa and Kosuke Namba :
Development of a mugineic acid family phytosiderophore analog as an iron fertilizer,
Nature Communications, 12, 1, 1558, 2021.

(要約): Iron (Fe) is an essential nutrient, but is poorly bioavailable because of its low solubility in alkaline soils; this leads to reduced agricultural productivity. To overcome this problem, we first showed that the soil application of synthetic 2'-deoxymugineic acid, a natural phytosiderophore from the Poaceae, can recover Fe deficiency in rice grown in calcareous soil. However, the high cost and poor stability of synthetic 2'-deoxymugineic acid preclude its agricultural use. In this work, we develop a more stable and less expensive analog, proline-2'-deoxymugineic acid, and demonstrate its practical synthesis and transport of its Fe-chelated form across the plasma membrane by Fe(III)·2'-deoxymugineic acid transporters. Possibility of its use as an iron fertilizer on alkaline soils is supported by promotion of rice growth in a calcareous soil by soil application of metal free proline-2'-deoxymugineic acid.
(キーワード): Azetidinecarboxylic Acid / Fertilizers / Iron / Siderophores / Soil
(徳島大学機関リポジトリ): ● Metadata: 2009105
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41467-021-21837-6
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33692352; ● Search Scopus @ Elsevier (PMID): 33692352; ● Search Scopus @ Elsevier (DOI): 10.1038/s41467-021-21837-6

(徳島大学機関リポジトリ: 2009105, DOI: 10.1038/s41467-021-21837-6, PubMed: 33692352) Suzu Endo, Akiko Suganami, Keijo Fukushima, Kanaho Senoo, Yumi Araki, W John Regan, Masato Mashimo, Yutaka Tamura and Hiromichi Fujino :
15-Keto-PGE 2 acts as a biased/partial agonist to terminate PGE 2-evoked signaling,
The Journal of Biological Chemistry, 295, 38, 13338-13352, 2020.

(要約): -evoked inflammation and/or maintaining homeostasis of colorectal tissues/cells functions.
(キーワード): Computer Simulation / Dinoprostone / HEK293 Cells / Humans / Inflammation / Models, Biological / Receptors, Prostaglandin E, EP2 Subtype / Receptors, Prostaglandin E, EP4 Subtype / Signal Transduction
(徳島大学機関リポジトリ): ● Metadata: 2009446
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.RA120.013988
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32727851; ● Search Scopus @ Elsevier (PMID): 32727851; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.RA120.013988

(徳島大学機関リポジトリ: 2009446, DOI: 10.1074/jbc.RA120.013988, PubMed: 32727851) Masaki Imanishi, Yusuke Yamakawa, Keijo Fukushima, Raiki Ikuto, Akiko Maegawa, Yuki Izawa-Ishizawa, Yuya Horinouchi, Masateru Kondo, Masatoshi Kishuku, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Koichiro Tsuchiya, Hiromichi Fujino, Koichi Tsuneyama and Keisuke Ishizawa :
Fibroblast-specific ERK5 deficiency changes tumor vasculature and exacerbates tumor progression in a mouse model.,
Naunyn-Schmiedeberg's Archives of Pharmacology, 393, 7, 1239-1250, 2020.

(要約): The roles of cancer-associated fibroblasts (CAFs) have been studied in the tumor progression, and CAFs are expected to become the new targets for cancer pharmacotherapies. CAFs contribute to tumor cell survival and proliferation, tumor angiogenesis, immune suppression, tumor inflammation, tumor cell invasion and metastasis, and extracellular matrix remodeling. However, detailed mechanisms of how CAFs function in the living system remain unclear. CAFs include α-smooth muscle actin, expressing activated fibroblasts similar to myofibroblasts, and are highly capable of producing collagen. Several reports have demonstrated the contributions of extracellular-signal-regulated kinase 5 (ERK5) in fibroblasts to the fibrotic processes; however, the roles of CAF-derived ERK5 remain unclear. To investigate the roles of CAF-derived ERK5 in the tumor progression, we created mice lacking the ERK5 gene specifically in fibroblasts. Colon-26 mouse colon cancer cells were implanted into the mice subcutaneously, and the histological analyses of the tumor tissue were performed after 2 weeks. Immunofluorescence analyses showed that recipient-derived fibroblasts existed within the tumor tissue. The present study demonstrated that fibroblast-specific ERK5 deficiency exacerbated tumor progression and it was accompanied with thicker tumor vessel formation and the increase in the number of activated fibroblasts. We combined the results of The Cancer Genome Atlas (TCGA) database analysis with our animal studies, and indicated that regulating ERK5 activity in CAFs or CAF invasion into the tumor tissue can be important strategies for the development of new targets in cancer pharmacotherapies.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00210-020-01859-5
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32307577; ● Search Scopus @ Elsevier (PMID): 32307577; ● Search Scopus @ Elsevier (DOI): 10.1007/s00210-020-01859-5

(DOI: 10.1007/s00210-020-01859-5, PubMed: 32307577) Hirofumi Hamano, Takahiro Niimura, Yuya Horinouchi, Yoshito Zamami, Kenshi Takechi, Mitsuhiro Goda, Masaki Imanishi, Masayuki Chuma, Yuki Izawa-Ishizawa, Licht Miyamoto, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Keisuke Ishizawa, Toshiaki Tamaki and Yasumasa Ikeda :
Proton pump inhibitors block iron absorption through direct regulation of hepcidin via the aryl hydrocarbon receptor-mediated pathway,
Toxicology Letters, 318, 86-91, 2020.

(要約): Proton pump inhibitors (PPIs) have been used worldwide to treat gastrointestinal disorders. A recent study showed that long-term use of PPIs caused iron deficiency; however, it is unclear whether PPIs affect iron metabolism directly. We investigated the effect of PPIs on the peptide hepcidin, an important iron regulatory hormone. First, we used the FDA Adverse Event Reporting System database and analyzed the influence of PPIs. We found that PPIs, as well as H2 blockers, increased the odds ratio of iron-deficient anemia. Next, HepG2 cells were used to examine the action of PPIs and H2 blockers on hepcidin. PPIs augmented hepcidin expression, while H2 blockers did not. In fact, the PPI omeprazole increased hepcidin secretion, and omeprazole-induced hepcidin upregulation was inhibited by gene silencing or the pharmacological inhibition of the aryl hydrocarbon receptor. In mouse experiments, omeprazole also increased hepatic hepcidin mRNA expression and blood hepcidin levels. In mice treated with omeprazole, protein levels of duodenal and splenic ferroportin decreased. Taken together, PPIs directly affect iron metabolism by suppressing iron absorption through the inhibition of duodenal ferroportin via hepcidin upregulation. These findings provide a new insight into the molecular mechanism of PPI-induced iron deficiency.
(徳島大学機関リポジトリ): ● Metadata: 2006818
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.toxlet.2019.10.016
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31669099; ● Search Scopus @ Elsevier (PMID): 31669099; ● Search Scopus @ Elsevier (DOI): 10.1016/j.toxlet.2019.10.016

(徳島大学機関リポジトリ: 2006818, DOI: 10.1016/j.toxlet.2019.10.016, PubMed: 31669099) Yoshito Zamami, Takahiro Niimura, Naoto Okada, Toshihiro Koyama, Keijo Fukushima, Yuki Izawa-Ishizawa and Keisuke Ishizawa :
Factors Associated With Immune Checkpoint Inhibitor-Related Myocarditis.,
JAMA Oncology, 2019.

(出版サイトへのリンク): ● Publication site (DOI): 10.1001/jamaoncol.2019.3113
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31436802; ● Search Scopus @ Elsevier (PMID): 31436802; ● Search Scopus @ Elsevier (DOI): 10.1001/jamaoncol.2019.3113

(DOI: 10.1001/jamaoncol.2019.3113, PubMed: 31436802) Naoki Kurata, Natsumi Tokashiki, Keijo Fukushima, Takaya Misao, Nanae Hasuoka, Kana Kitagawa, Masato Mashimo, W John Regan, Toshihiko Murayama and Hiromichi Fujino :
Short chain fatty acid butyrate uptake reduces expressions of prostanoid EP4 receptors and their mediation of cyclooxygenase-2 induction in HCA-7 human colon cancer cells.,
European Journal of Pharmacology, 853, 308-315, 2019.

(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ejphar.2019.04.014
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30980797; ● Search Scopus @ Elsevier (PMID): 30980797; ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2019.04.014

(DOI: 10.1016/j.ejphar.2019.04.014, PubMed: 30980797) Hirofumi Hamano, Marin Mitsui, Yoshito Zamami, Kenshi Takechi, Takahiro Nimura, Naoto Okada, Keijo Fukushima, Masaki Imanishi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasushi Kirino, Toshimi Nakamura, Kazuhiko Teraoka, Yasumasa Ikeda, Hiromichi Fujino, Hiroaki Yanagawa, Toshiaki Tamaki and Keisuke Ishizawa :
Irinotecan-induced neutropenia is reduced by oral alkalization drugs: analysis using retrospective chart reviews and the spontaneous reporting database.,
Supportive Care in Cancer, 27, 3, 849-856, 2019.

(要約): These data indicate that oral alkalization drugs may reduce the frequency of neutropenia caused by irinotecan administration, making it possible to increase the dose safely.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00520-018-4367-y
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30062585; ● Search Scopus @ Elsevier (PMID): 30062585; ● Search Scopus @ Elsevier (DOI): 10.1007/s00520-018-4367-y

(DOI: 10.1007/s00520-018-4367-y, PubMed: 30062585) Masateru Kondo, Masaki Imanishi, Keijo Fukushima, Raiki Ikuto, Yoichi Murai, Yuya Horinouchi, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa :
Xanthine Oxidase Inhibition by Febuxostat in Macrophages Suppresses Angiotensin II-induced Aortic Fibrosis.,
American Journal of Hypertension, 32, 3, 249-256, 2019.

(要約): Our results suggested that FEB ameliorates Ang II-induced aortic fibrosis via suppressing macrophage-derived TGF-1 expression.
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/ajh/hpy157
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30351343; ● Search Scopus @ Elsevier (PMID): 30351343; ● Search Scopus @ Elsevier (DOI): 10.1093/ajh/hpy157

(DOI: 10.1093/ajh/hpy157, PubMed: 30351343) Naofumi Seira, Kazuyuki Yamagata, Keijo Fukushima, Yumi Araki, Naoki Kurata, Naoki Yanagisawa, Masato Mashimo, Hiroyuki Nakamura, W John Regan, Toshihiko Murayama and Hiromichi Fujino :
Cellular density-dependent increases in HIF-1α compete with c-Myc to down-regulate human EP4 receptor promoter activity through Sp-1-binding region.,
Pharmacology Research & Perspectives, 6, 6, 2018.

(要約): The up-regulated expression of E-type prostanoid (EP) 4 receptors has been implicated in carcinogenesis; however, the expression of EP4 receptors has also been reported to be weaker in tumor tissues than in normal tissues. Indeed, EP4 receptors have been suggested to play a role in the maintenance of colorectal homeostasis. This study aimed to examine the underlying mechanisms/reasons for why inconsistent findings have been reported regarding EP4 receptor expression levels in homeostasis and carcinogenesis by focusing on cellular densities. Thus, the human colon cancer HCA-7 cells, which retain some functional features of normal epithelia, and luciferase reporter genes containing wild-type or mutated EP4 receptor promoters were used for elucidating the cellular density-dependent mechanisms about the regulation of EP4 receptor expression. In silico analysis was also utilized for confirming the relevance of the findings with respect to colon cancer development. We here demonstrated that the expression of EP4 receptors was up-regulated by c-Myc by binding to Sp-1 under low cellular density conditions, but was down-regulated under high cellular density conditions via the increase in the expression levels of HIF-1α protein, which may pull out c-Myc and Sp-1 from DNA-binding. The tightly regulated EP4 receptor expression mechanism may be a critical system for maintaining homeostasis in normal colorectal epithelial cells. Therefore, once the system is altered, possibly due to the transient overexpression of EP4 receptors, it may result in aberrant cellular proliferation and transformation to cancerous phenotypes. However, at the point, EP4 receptors themselves and their mediated homeostasis would be no longer required.
(キーワード): Carcinogenesis / Cell Count / Cell Line, Tumor / Colonic Neoplasms / Computational Biology / Down-Regulation / Gene Expression Regulation, Neoplastic / Humans / Hypoxia-Inducible Factor 1, alpha Subunit / Promoter Regions, Genetic / Proto-Oncogene Proteins c-myc / Receptors, Prostaglandin E, EP4 Subtype / Sp1 Transcription Factor / Up-Regulation
(徳島大学機関リポジトリ): ● Metadata: 2008609
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/prp2.441
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30455960; ● Search Scopus @ Elsevier (PMID): 30455960; ● Search Scopus @ Elsevier (DOI): 10.1002/prp2.441

(徳島大学機関リポジトリ: 2008609, DOI: 10.1002/prp2.441, PubMed: 30455960) Masaki Imanishi, Yuki Izawa-Ishizawa, T Sakurada, Y Kohara, Yuya Horinouchi, E Sairyo, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yasumasa Ikeda, Hiromichi Fujino, M Yoshizumi, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa :
Nitrosonifedipine, a Photodegradation Product of Nifedipine, Suppresses Pharmacologically Induced Aortic Aneurysm Formation.,
Pharmacology, 102, 5-6, 281-286, 2018.

(要約): We have reported that nitrosonifedipine (NO-NIF), a photodegradation product of nifedipine, has strong antioxidant and endothelial protective effects, and can suppress several cardiovascular diseases in animal models. The objective of the present study was to investigate the effects of NO-NIF on aortic aneurysm formation. The mice were infused with β-aminopropionitrile for 2 weeks and angiotensin II for 6 weeks to induce aortic aneurysm formation. The oxidative stress was measured by dihydroethidium staining and nitrotyrosine staining. The expressions of inflammation-related genes were assessed by quantitative real-time PCR and immunohistochemical staining. To clarify the mechanisms of how NO-NIF suppresses vascular cell adhesion molecule (VCAM)-1, endothelial cells were used in in vitro system. NO-NIF suppressed pharmacologically induced the aortic aneurysm formation and aortic expansion without blood pressure changes. NO-NIF suppressed elastin degradation and matrix metalloproteinase-2 mRNA expression. NO-NIF suppressed the reactive oxygen species-cyclophilin A positive feedback loop. Upregulated mRNA expressions of inflammation-related genes and endothelial VCAM-1 were suppressed by NO-NIF co-treatment in aortae. NO-NIF has the potential to be a new, nifedipine-derived therapeutic drug for suppressing aortic aneurysm formation by directly improving aortic structure with its strong ability to reduce oxidative stress and inflammation.
(キーワード): Aminopropionitrile / Angiotensin II / Animals / Antigens, Differentiation / Antioxidants / Aortic Aneurysm / Chemokine CCL2 / Cyclophilins / Disease Models, Animal / Elastin / Endothelial Cells / Human Umbilical Vein Endothelial Cells / Humans / Male / Matrix Metalloproteinase 2 / Mice / Nifedipine / Nitroso Compounds / Oxidative Stress / Photolysis / Reactive Oxygen Species / Vascular Cell Adhesion Molecule-1
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000492577
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30253416; ● Summary page in Scopus @ Elsevier: 2-s2.0-85054191604

(DOI: 10.1159/000492577, PubMed: 30253416, Elsevier: Scopus) Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki :
Renoprotective effects of a factor Xa inhibitor: fusion of basic research and a database analysis.,
Scientific Reports, 8, 1, 2018.

(要約): Renal tubulointerstitial injury, an inflammation-associated condition, is a major cause of chronic kidney disease (CKD). Levels of activated factor X (FXa), a blood coagulation factor, are increased in various inflammatory diseases. Therefore, we investigated the protective effects of an FXa inhibitor against renal tubulointerstitial injury using unilateral ureteral obstruction (UUO) mice (a renal tubulointerstitial fibrosis model) and the Food and Drug Administration Adverse Events Reporting System (FAERS) database. The renal expression levels of FX and the FXa receptors protease-activated receptor (PAR)-1 and PAR-2 were significantly higher in UUO mice than in sham-operated mice. UUO-induced tubulointerstitial fibrosis and extracellular matrix expression were suppressed in UUO mice treated with the FXa inhibitor edoxaban. Additionally, edoxaban attenuated UUO-induced macrophage infiltration and inflammatory molecule upregulation. In an analysis of the FAERS database, there were significantly fewer reports of tubulointerstitial nephritis for patients treated with FXa inhibitors than for patients not treated with inhibitors. These results suggest that FXa inhibitors exert protective effects against CKD by inhibiting tubulointerstitial fibrosis.
(徳島大学機関リポジトリ): ● Metadata: 2005594
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-018-29008-2
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30022146; ● Search Scopus @ Elsevier (PMID): 30022146; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-018-29008-2

(徳島大学機関リポジトリ: 2005594, DOI: 10.1038/s41598-018-29008-2, PubMed: 30022146) Takahiro Niimura, Yoshito Zamami, Toshihiro Koyama, Yuki Izawa-Ishizawa, Masashi Miyake, Tadashi Koga, Keisaku Harada, Ayako Ohshima, Toru Imai, Yutaka Kondo, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki, Shiro Hinotsu, R Mitsunobu Kano and Keisuke Ishizawa :
Hydrocortisone administration was associated with improved survival in Japanese patients with cardiac arrest.,
Scientific Reports, 7, 1, 2017.

(要約): There are few reports on hydrocortisone administration after cardiac arrest, and those that have been published included few subjects. This study aimed to evaluate the effect of hydrocortisone administration on the outcomes of patients who experienced cardiac arrest. We investigated the survival discharge rates and the length of hospital stay from cardiac arrest to discharge, stratified by use of hydrocortisone, using a Japanese health-insurance claims dataset that covers approximately 2% of the Japanese population. The study included the data of 2233 subjects who experienced either in-hospital or out-of-hospital cardiac arrest between January 2005 and May 2014. These patients were divided into two groups, based on the administration of hydrocortisone. We adjusted the baseline characteristics, medical treatment, and drug administration data of the two groups using propensity scores obtained via the inverse probability of treatment weighted method. The hydrocortisone group had a significantly higher survival discharge rate (13/61 [21.1%] vs. 240/2172 [11.0%], adjusted odds ratio: 4.2, 95% CI: 1.60-10.98, p = 0.004). In addition, the administration of hydrocortisone was independent predictor of survival to discharge (hazard ratio: 4.6, p < 0.001). The results demonstrate a correlation between hydrocortisone administration and the high rates of survival to discharge.
(徳島大学機関リポジトリ): ● Metadata: 2005547
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-017-17686-3
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29263333; ● Search Scopus @ Elsevier (PMID): 29263333; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-017-17686-3

(徳島大学機関リポジトリ: 2005547, DOI: 10.1038/s41598-017-17686-3, PubMed: 29263333) Araki Yumi, Suganami Akiko, Endo Suzu, Masuda Yuta, Keijo Fukushima, Regan W. John, Murayama Toshihiko, Tamura Yutaka and Hiromichi Fujino :
PGE1 and E3 show lower efficacies than E2 to -catenin-mediated activity as biased ligands of EP4 prostanoid receptors.,
FEBS Letters, 591, 22, 3771-3780, 2017.

(要約): The 2-series of prostaglandin E (PGE ) is regarded as a pro-cancer prostanoid, whereas the 1-series (PGE ) and the 3-series (PGE ) are considered to act as anti-cancer prostanoids. In the present study, we provide possible reasons why PGE and PGE , but not PGE , exert anti-cancer effects by focusing on each diverged E-type prostanoid (EP)4 receptor-mediated signaling pathway. PGE , PGE and PGE function as full agonists in terms of G - and G -protein-mediated signaling. However, PGE and PGE function as partial agonists of T-cell factor (TCF)/β-catenin (β-cat)-mediated activity, the well-known cancer-related signaling pathway. Furthermore, pretreatment with PGE or PGE almost completely reduces PGE -induced TCF/β-cat activity. These results provide a plausible reason why PGE and PGE function as anti-cancer prostanoids as a result of novel biased activity for EP4 receptors.
(キーワード): Alprostadil / Binding Sites / Crystallography, X-Ray / Dinoprostone / Gene Expression Regulation / HEK293 Cells / Humans / Hydrogen Bonding / Ligands / Models, Molecular / Protein Binding / Receptors, Prostaglandin E, EP4 Subtype / Signal Transduction / beta Catenin
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/1873-3468.12878
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28986997; ● Search Scopus @ Elsevier (PMID): 28986997; ● Search Scopus @ Elsevier (DOI): 10.1002/1873-3468.12878

(DOI: 10.1002/1873-3468.12878, PubMed: 28986997) Tadanobu Takahashi, Takashi Agarikuchi, Yuuki Kurebayashi, Nona Shibahara, Chihiro Suzuki, Akiko Kishikawa, Keijo Fukushima, Maiko Takano, Fumie Suzuki, Hirohisa Wada, Tadamune Otsubo, Kiyoshi Ikeda, Akira Minami and Takashi Suzuki :
Easy and rapid detection of mumps virus by live fluorescent visualization of virus-infected cells,
PLoS ONE, 10, 12, e0144038, 2015.

(要約): Mumps viruses show diverse cytopathic effects (CPEs) of infected cells and viral plaque formation (no CPE or no plaque formation in some cases) depending on the viral strain, highlighting the difficulty in mumps laboratory studies. In our previous study, a new sialidase substrate, 2-(benzothiazol-2-yl)-4-bromophenyl 5-acetamido-3,5-dideoxy-α-D-glycero-D-galacto-2-nonulopyranosidonic acid (BTP3-Neu5Ac), was developed for visualization of sialidase activity. BTP3-Neu5Ac can easily and rapidly perform histochemical fluorescent visualization of influenza viruses and virus-infected cells without an antiviral antibody and cell fixation. In the present study, the potential utility of BTP3-Neu5Ac for rapid detection of mumps virus was demonstrated. BTP3-Neu5Ac could visualize dot-blotted mumps virus, virus-infected cells, and plaques (plaques should be called focuses due to staining of infected cells in this study), even if a CPE was not observed. Furthermore, virus cultivation was possible by direct pick-up from a fluorescent focus. In conventional methods, visible appearance of the CPE and focuses often requires more than 6 days after infection, but the new method with BTP3-Neu5Ac clearly visualized infected cells after 2 days and focuses after 4 days. The BTP3-Neu5Ac assay is a precise, easy, and rapid assay for confirmation and titration of mumps virus.
(キーワード): Animals / Chlorocebus aethiops / Fluorescence / Humans / Mumps virus / Vero Cells
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0144038
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26629699; ● Summary page in Scopus @ Elsevier: 2-s2.0-84955490418

(DOI: 10.1371/journal.pone.0144038, PubMed: 26629699, Elsevier: Scopus) Keijo Fukushima, Tadanobu Takahashi, Hiroo Ueyama, Masahiro Takaguchi, Seigo Ito, Kenta Oishi, Akira Minami, Erika Ishitsubo, Hiroaki Tokiwa, Toru Takimoto and Takashi Suzuki :
Amino acid substitutions contributing to α2,6-sialic acid linkage binding specificity of human parainfluenza virus type 3 hemagglutinin-neuraminidase,
FEBS Letters, 589, 11, 1278-1282, 2015.

(要約): Human parainfluenza virus type 3 (hPIV3) recognizes both α2,3- and α2,6-linked sialic acids, whereas human parainfluenza virus type 1 (hPIV1) recognizes only α2,3-linked sialic acids. To identify amino acid residues that confer α2,6-linked sialic acid recognition of hPIV3, amino acid residues in or neighboring the sialic acid binding pocket of the hPIV3 hemagglutinin-neuraminidase (HN) glycoprotein were substituted for the corresponding residues of hPIV1 HN. Hemadsorption assay with sialyl linkage-modified red blood cells indicated that amino acid residues at positions 275, 277, 372, and 426 contribute to α2,6-linked sialic acid recognition of the HN3 glycoprotein.
(キーワード): Hemagglutinin-neuraminidase / HN / Human parainfluenza virus / Receptor binding / Sialic acid / Sialyl linkage
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.febslet.2015.03.036
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25871520; ● Summary page in Scopus @ Elsevier: 2-s2.0-84936769300

(DOI: 10.1016/j.febslet.2015.03.036, PubMed: 25871520, Elsevier: Scopus) Tomohiro Kawahara, Tadanobu Takahashi, Kenta Oishi, Hiromu Tanaka, Midori Masuda, Shunsaku Takahashi, Maiko Takano, Tatsuya Kawakami, Keijo Fukushima, Hiroaki Kanazawa and Takashi Suzuki :
Consecutive oral administration of Bifidobacterium longum MM-2 improves the defense system against influenza virus infection by enhancing natural killer cell activity in a murine model,
Microbiology and Immunology, 59, 1, 1-12, 2015.

(要約): Bifidobacterium, one of the major components of intestinal microflora, shows anti-influenza virus (IFV) potential as a probiotic, partly through enhancement of innate immunity by modulation of the intestinal immune system. Bifidobacterium longum MM-2 (MM-2), a very safe bacterium in humans, was isolated from healthy humans and its protective effect against IFV infection in a murine model shown. In mice that were intranasally inoculated with IFV, oral administration of MM-2 for 17 consecutive days improved clinical symptoms, reduced mortality, suppressed inflammation in the lower respiratory tract, and decreased virus titers, cell death, and pro-inflammatory cytokines such as IL-6 and TNF-α in bronchoalveolar lavage fluid. The anti-IFV mechanism of MM-2 involves innate immunity through significant increases in NK cell activities in the lungs and spleen and a significant increase in pulmonary gene expression of NK cell activators such as IFN-γ, IL-2, IL-12 and IL-18. Even in non-infected mice, MM-2 administration also induced significant enhancement of both IFN-γ production by Peyer's patch cells (PPs) and splenetic NK cell activity. Oral administration of MM-2 for 17 days activates systemic immunoreactivity in PPs, which contributes to innate immunity, including NK cell activation, resulting in an anti-IFV effect. MM-2 as a probiotic may function as a prophylactic agent in the management of an IFV epidemic.
(キーワード): Bifidobacterium longum / Influenza virus / Natural killer cell / Probiotics
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/1348-0421.12210
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25400245; ● Summary page in Scopus @ Elsevier: 2-s2.0-84927741155

(DOI: 10.1111/1348-0421.12210, PubMed: 25400245, Elsevier: Scopus) Tadanobu Takahashi, Maiko Takano, Yuuki Kurebayashi, Takashi Agarikuchi, Chihiro Suzuki, Keijo Fukushima, Shunsaku Takahashi, Tadamune Otsubo, Kiyoshi Ikeda, Akira Minami and Takashi Suzuki :
Rapid fluorescent detection assay for human parainfluenza viruses,
Biological & Pharmaceutical Bulletin, 38, 8, 1214-1219, 2015.

(要約): Human parainfluenza virus type 1 (hPIV1) does not form clear plaque by the conventional plaque formation assay because of slightly a cytopathic effects in many cell lines infected with hPIV1, thus making in virus titration, isolation and inhibitor evaluation difficult. We have succeeded in fluorescent histochemical visualization of sialidase activities of influenza A and B viruses, Newcastle disease virus and Sendai virus by using a novel fluorescent sialidase substrate, 2-(benzothiazol-2-yl)-4-bromophenyl 5-acetamido-3,5-dideoxy-α-D-glycero-D-galacto-2-nonulopyranosidonic acid (BTP3-Neu5Ac). In this study, we applied the BTP3-Neu5Ac assay for rapid detection of hPIV1 and hPIV type 3. The BTP3-Neu5Ac assay could histochemically visualize dot-blotted hPIVs on a membrane and hPIV-infected cells as local fluorescence under UV irradiation. We succeeded in distinct fluorescent visualization of hPIV1-infected cells in only 3 d using the BTP3-Neu5Ac assay. Due to there being no fixation, hPIV1 was isolated directly from fluorescent stained focus cells by the BTP3-Neu5Ac assay. Establishment of a sensitive, easy, and rapid fluorescent focus detection assay for hPIV, hPIV1 in particular will contribute greatly to progress in hPIV studies.
(キーワード): 2-(benzothiazol-2-yl)-4-bromophenyl 5-acetamido-3,5-dideoxy-α-D-glycero-D-galacto-2-nonulopyranosidonic acid (BTP3-Neu5A) / Fluorescent visualization / Histochemical staining / Human parainfluenza virus (hPIV) / Sialidase activity
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b15-00298
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26235585; ● Summary page in Scopus @ Elsevier: 2-s2.0-84940909120

(DOI: 10.1248/bpb.b15-00298, PubMed: 26235585, Elsevier: Scopus) Keijo Fukushima, Tadanobu Takahashi, Seigo Ito, Masahiro Takaguchi, Maiko Takano, Yuuki Kurebayashi, Kenta Oishi, Akira Minami, Tatsuya Kato, Y. Enoch Park, Hidekazu Nishimura, Toru Takimoto and Takashi Suzuki :
Terminal sialic acid linkages determine different cell infectivities of human parainfluenza virus type 1 and type 3,
Virology, 464-465, 1, 424-431, 2014.

(要約): Human parainfluenza virus type 1 (hPIV1) and type 3 (hPIV3) initiate infection by sialic acid binding. Here, we investigated sialic acid linkage specificities for binding and infection of hPIV1 and hPIV3 by using sialic acid linkage-modified cells treated with sialidases or sialyltransferases. The hPIV1 is bound to only α2,3-linked sialic acid residues, whereas hPIV3 is bound to α2,6-linked sialic acid residues in addition to α2,3-linked sialic acid residues in human red blood cells. α2,3 linkage-specific sialidase treatment of LLC-MK2 cells and A549 cells decreased the infectivity of hPIV1 but not that of hPIV3. Treatment of A549 cells with α2,3 linkage-specific sialyltransferase increased infectivities of both hPIV1 and hPIV3, whereas α2,6 linkage-specific sialyltransferase treatment increased only hPIV3 infectivity. Clinical isolates also showed similar sialic acid linkage specificities. We concluded that hPIV1 utilizes only α2,3 sialic acid linkages and that hPIV3 makes use of α2,6 sialic acid linkages in addition to α2,3 sialic acid linkages as viral receptors.
(キーワード): HPIV1 / HPIV3 / Human parainfluenza virus / Receptor specificity / Sialic acid / Sialic acid linkages
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.virol.2014.07.033
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25146600; ● Summary page in Scopus @ Elsevier: 2-s2.0-84919776201

(DOI: 10.1016/j.virol.2014.07.033, PubMed: 25146600, Elsevier: Scopus) Tadanobu Takahashi, Kazuhiko Ito, Keijo Fukushima, Masahiro Takaguchi, Takuya Hayakawa, Yasuo Suzuki and Takashi Suzuki :
Sulfatide negatively regulates the fusion process of human parainfluenza virus type 3,
The Journal of Biochemistry, 152, 4, 373-380, 2012.

(要約): Sulfatide (HSO(3)-3-galactosylceramide), which enriched in lipid rafts of plasma membranes in various epithelial cell lines, is a critical component of host cells for effective production of influenza A virus. However, the function of sulfatide in other virus infections targeting epithelial cells remains unknown. In this study, the effect of sulfatide on infection of human parainfluenza virus type 3 (hPIV3) was demonstrated by using genetically produced sulfatide-enriched cells and by treatment of hPIV3-infected cells with anti-sulfatide monoclonal antibody (GS-5) as well as by addition of sulfatide to the cells. hPIV3 was found to bind to sulfatide in a virus overlay assay and a solid-phase binding assay. Genetic expression of sulfatide in COS-7 cells defective in sulfatide suppressed initial hPIV3 infection and formation of multinucleate virus-infected cells. Treatment of virus-infected LLC-MK2 cells with GS-5 promoted formation of multinucleate cells. In contrast, exogenous addition of sulfatide to hPIV3-infected COS-7 cells and cells expressing the hPIV3-hemagglutinin-neuraminidase (HN) gene and fusion (F) gene conspicuously reduced the formation of multinucleate cells. The results suggest that sulfatide negatively regulates the fusion process of hPIV3, possibly through interaction with HN or F glycoprotein on the cell surface.
(キーワード): fusion / human parainfluenza virus type 3 / infection / sulfatide / transferase
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/jb/mvs080
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22821828; ● Summary page in Scopus @ Elsevier: 2-s2.0-84866890922

(DOI: 10.1093/jb/mvs080, PubMed: 22821828, Elsevier: Scopus) Keijo Fukushima, Tadanobu Takahashi, Masahiro Takaguchi, Hiroo Ueyama, Seigo Ito, Yuuki Kurebayashi, Tomohiro Kawanishi, Lois Jennifer Mckimm-Breschkin, Toru Takimoto, Akira Minami and Takashi Suzuki :
Plaque formation assay for human parainfluenza virus type 1,
Biological & Pharmaceutical Bulletin, 34, 7, 996-1000, 2011.

(要約): Human parainfluenza virus type 1 (hPIV1) generally does not show visible plaques in common cell lines, including Lewis lung carcinoma-monkey kidney (LLC-MK(2)) cells, by plaque formation assays for human parainfluenza virus type 3 (hPIV3) and Sendai virus. In several conditions of the plaque formation assay, complete elimination of serum proteins in the overlay medium was necessary for visualization of hPIV1-induced plaque formation in LLC-MK(2) cells. We developed a plaque formation assay for hPIV1 isolation and titration in LLC-MK(2) cells using an initial overlay medium of bovine serum albumin-free Eagle's minimum essential medium containing agarose and acetylated trypsin for 4-6 d followed by a second overlay staining medium containing agarose and neutral red. The assay allowed both laboratory and clinical hPIV1 strains to form large plaques. The plaque reduction assay was also performed with rabbit anti-hPIV1 antibody as a general evaluation model of viral inhibitors to decrease both the plaque number and size. The results indicate that the plaque formation assay is useful for hPIV1 isolation, titration, evaluation of antiviral reagents and epidemiologic research.
(キーワード): Antiviral reagent / Human parainfluenza virus type 1 / Isolation / Lewis lung carcinoma-monkey kidney cell / Plaque assay
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.34.996
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21720003; ● Summary page in Scopus @ Elsevier: 2-s2.0-79960293059

(DOI: 10.1248/bpb.34.996, PubMed: 21720003, Elsevier: Scopus) Masahiro Takaguchi, Tadanobu Takahashi, Chika Hosokawa, Hiroo Ueyama, Keijo Fukushima, Takuya Hayakawa, Kazuhiko Itoh, Kiyoshi Ikeda and Takashi Suzuki :
A single amino acid mutation at position 170 of human parainfluenza virus type 1 fusion glycoprotein induces obvious syncytium formation and caspase-3-dependent cell death,
The Journal of Biochemistry, 149, 2, 191-202, 2010.

(要約): An escape mutant of human parainfluenza virus type 1 (hPIV1), which was selected by serial passage in the presence of a sialidase inhibitor, 4-O-thiocarbamoylmethyl-2-deoxy-2,3-didehydro-N-acetylneur-aminic acid (TCM-Neu5Ac2en), exhibited remarkable syncytium formation and virus-induced cell death in LLC-MK2 cells but no difference in susceptibility for the sialidase inhibitor TCM-Neu5Ac2en from that of wild-type hPIV1 strain C35 (WT). The mutant virus also had higher replication and plaque formation abilities. The mutant virus acquired two amino acid mutations, Glu to Gly at position 170 and Ala to Glu 442 in fusion (F) glycoprotein, but no mutations in haemaggulutinin-neuraminidase (HN) glycoprotein. Using cells co-expressing F and HN genes with site-specific mutagenesis, we demonstrated that a point mutation of Glu to Gly at position 170, which was estimated to be located in hPIV1 F glycoprotein heptad repeat 1, was required for obvious syncytium formation and caspase-3-dependent cell death. In contrast, wild-type F glycoprotein induced no synctium formation or cell death. The findings suggest that a single amino acid mutation of hPIV1 F glycoprotein promotes syncytium formation that is followed by caspase-3-dependent cell death.
(キーワード): Fusion protein / heptad repeat / human parainfluenza virus / membrane fusion / sialidase inhibitor
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/jb/mvq139
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21186250; ● Summary page in Scopus @ Elsevier: 2-s2.0-79251524885

(DOI: 10.1093/jb/mvq139, PubMed: 21186250, Elsevier: Scopus) Tadanobu Takahashi, Yuuki Kurebayashi, Kumiko Ikeya, Takashi Mizuno, Keijo Fukushima, Hiroko Kawamoto, Yoshihiro Kawaoka, Yasuo Suzuki and Takashi Suzuki :
The low-pH stability discovered in neuraminidase of 1918 pandemic influenza A virus enhances virus replication,
PLoS ONE, 5, 12, e15556, 2010.

(要約): The "Spanish" pandemic influenza A virus, which killed more than 20 million worldwide in 1918-19, is one of the serious pathogens in recorded history. Characterization of the 1918 pandemic virus reconstructed by reverse genetics showed that PB1, hemagglutinin (HA), and neuraminidase (NA) genes contributed to the viral replication and virulence of the 1918 pandemic influenza virus. However, the function of the NA gene has remained unknown. Here we show that the avian-like low-pH stability of sialidase activity discovered in the 1918 pandemic virus NA contributes to the viral replication efficiency. We found that deletion of Thr at position 435 or deletion of Gly at position 455 in the 1918 pandemic virus NA was related to the low-pH stability of the sialidase activity in the 1918 pandemic virus NA by comparison with the sequences of other human N1 NAs and sialidase activity of chimeric constructs. Both amino acids were located in or near the amino acid resides that were important for stabilization of the native tetramer structure in a low-pH condition like the N2 NAs of pandemic viruses that emerged in 1957 and 1968. Two reverse-genetic viruses were generated from a genetic background of A/WSN/33 (H1N1) that included low-pH-unstable N1 NA from A/USSR/92/77 (H1N1) and its counterpart N1 NA in which sialidase activity was converted to a low-pH-stable property by a deletion and substitutions of two amino acid residues at position 435 and 455 related to the low-pH stability of the sialidase activity in 1918 NA. The mutant virus that included "Spanish Flu"-like low-pH-stable NA showed remarkable replication in comparison with the mutant virus that included low-pH-unstable N1 NA. Our results suggest that the avian-like low-pH stability of sialidase activity in the 1918 pandemic virus NA contributes to the viral replication efficiency.
(キーワード): Amino Acids / Animals / Cell Line / Dogs / Flow Cytometry / Humans / Hydrogen-Ion Concentration / Influenza A virus / Models, Genetic / Neuraminidase / Pandemics / Plasmids / Protein Conformation / Virus Replication
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0015556
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21151571; ● Summary page in Scopus @ Elsevier: 2-s2.0-78650125730

(DOI: 10.1371/journal.pone.0015556, PubMed: 21151571, Elsevier: Scopus) Kumer Repon Saha, Tadanobu Takahashi, Yuuki Kurebayashi, Keijo Fukushima, Akira Minami, Noriaki Kinbara, Masaki Ichitani, M. Yuko Sagesaka and Takashi Suzuki :
Antiviral effect of strictinin on influenza virus replication,
Antiviral Research, 88, 1, 10-18, 2010.

(要約): Strictinin, which is a member of the ellagitanin family of hydrolyzable tannins, prevented replication of human, duck and swine influenza A viruses (IAVs) in vitro at non-toxic concentrations. The addition of strictinin at the same time as IAV inoculation to MDCK cells inhibited viral replication in a dose-dependent manner. Strictinin showed 50% inhibitory concentrations for IAVs from 0.09±0.021 to 0.28±0.037μM (mean±S.E.M.) by the focus-forming assay. Treatment of MDCK cells with strictinin before and after viral inoculation resulted in no significant antiviral activity. Further studies showed that strictinin inhibited IAV-induced hemifusion. However, strictinin exhibited no inhibitory effect against receptor binding, sialidase activity. Strictinin also showed an antiviral effect on influenza B virus and human parainfluenza virus type-1 in vitro. The results indicate that strictinin is a useful antiviral agent.
(キーワード): Antiviral / Influenza / Parainfluenza / Strictinin / Viral entry / Virus
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.antiviral.2010.06.008
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20615432; ● Summary page in Scopus @ Elsevier: 2-s2.0-77956917225

(DOI: 10.1016/j.antiviral.2010.06.008, PubMed: 20615432, Elsevier: Scopus)

MISC

Keijo Fukushima, Tadanobu Takahashi and Takashi Suzuki :
Characterization of Human Parainfluenza Virus Receptor Using Terminal Sialic Acid Linkage-Modified Cells.,
Methods in Molecular Biology, 2556, 169-178, 2022.

(要約): Human parainfluenza virus type 1 (hPIV1) and type 3 (hPIV3) are respiratory pathogen viruses that bind to terminal sialic acids of glycoconjugates on the cell surface hemagglutinin-neuraminidase glycoprotein. Sialic acid residues are linked to the galactose residue primarily by α2,3 or α2,6 linkages on the terminal of glycoprotein or glycolipids. One of the major determinants of pathogenicity or tissue tropism is virus binding or infection specificity for each sialyl linkage. Sialic linkage-modified human blood cells or mammalian cells that mainly have α2,3- or α2,6-linked sialic acid residues on the surface can be prepared by treatment with linkage-specific sialidases or sialyltransferases. These linkage-modified cells can be used in hemagglutination assays to estimate virus particles' binding specificity, hemadsorption assays to estimate virus glycoproteins' binding specificity, and virus infectivity assays. These methods contribute to identifying the specificity of sialic acid lineage recognition of the hPIV or other sialic acid-binding viruses.
(キーワード): Animals / Galactose / Glycolipids / HN Protein / Humans / Mammals / Membrane Glycoproteins / N-Acetylneuraminic Acid / Parainfluenza Virus 1, Human / Paramyxoviridae Infections / Receptors, Virus / Sialyltransferases
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/978-1-0716-2635-1_13
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36175634; ● Search Scopus @ Elsevier (PMID): 36175634; ● Search Scopus @ Elsevier (DOI): 10.1007/978-1-0716-2635-1_13

(DOI: 10.1007/978-1-0716-2635-1_13, PubMed: 36175634) Masato Mashimo, Asuka Shimizu, Aimi Mori, Ayaka Hamaguchi, Keijo Fukushima, Naofumi Seira, Takeshi Fujii and Hiromichi Fujino :
PARP14 regulates EP4 receptor expression in human colon cancer HCA-7 cells.,
Biochemical and Biophysical Research Communications, 623, 133-139, 2022.

(要約): E type prostanoid 4 (EP4) receptors and their signaling pathways have been implicated in the development and malignant transformation of colorectal cancer. We herein demonstrated that the mono(ADP-ribosyl)ation of histone deacetylase (HDAC)1 and HDAC2 by poly(ADP-ribose) polymerase 14 (PARP14) may be required to induce the expression of EP4 receptors. The suppression of PARP14 activity by siRNA and/or its inhibitors reduced the mRNA expression of EP4 receptors. Thus, the expression of their proteins to approximately 50-80% in human colon cancer HCA-7 cells, however, which retained the activities of EP4 receptors to some extent. Since the expression levels of EP4 receptors are important factors for the maintenance of homeostasis, the adequate inhibition of PARP14 activity will be a good target for the prevention of colon cancer and/or as an alternative therapy for this disease. Since non-steroidal anti-inflammatory drugs (NSAIDs) are associated with a risk of heart attacks and stroke, novel PARP14 inhibitors will supersede NSAIDs without causing heart attacks and stroke, while maintaining appropriate EP4 receptor-mediated intestinal homeostasis.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2022.07.055
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35914351; ● CiNii @ 国立情報学研究所 (CRID): 1360861707370271744; ● Summary page in Scopus @ Elsevier: 2-s2.0-85135092033

(DOI: 10.1016/j.bbrc.2022.07.055, PubMed: 35914351, CiNii: 1360861707370271744, Elsevier: Scopus) Keijo Fukushima, Tadanobu Takahashi, Masahiro Takaguchi, Seigo Ito, Chihiro Suzuki, Takashi Agarikuchi, Yuuki Kurebayashi, Akira Minami and Takashi Suzuki :
A I131V Substitution in the Fusion Glycoprotein of Human Parainfluenza Virus Type 1 Enhances Syncytium Formation and Virus Growth.,
Biological & Pharmaceutical Bulletin, 42, 5, 827-832, 2019.

(要約): Human parainfluenza virus type 1 (hPIV1) has two spike glycoproteins, the hemagglutinin-neuraminidase (HN) glycoprotein as a receptor-binding protein and the fusion (F) glycoprotein as a membrane-fusion protein. The F glycoprotein mediates both membrane fusion between the virus and cell and membrane fusion between cells, called syncytium formation. Wild-type C35 strain (WT) of hPIV1 shows little syncytium formation of infected cells during virus growth. In the present study, we isolated a variant virus (Vr) from the WT that showed enhanced syncytium formation of infected cells by using our previously established hPIV1 plaque formation assay. Vr formed a larger focus and showed increased virus growth compared with WT. Sequence analysis of the spike glycoprotein genes showed that the Vr had a single amino acid substitution of Ile to Val at position 131 in the fusion peptide region of the F glycoprotein without any substitutions of the HN glycoprotein. The Vr F glycoprotein showed enhanced syncytium formation in F and HN glycoprotein-expressing cells. Additionally, expression of the Vr F glycoprotein increased the focus area of the WT-infected cells. The single amino acid substitution at position 131 in the F glycoprotein of hPIV1 gives hPIV1 abilities to enhance syncytium formation and increase cell-to-cell spread. The present study supports the possibility that hPIV1 acquires increased virus growth in vitro from promotion of direct cell-to-cell transmission by syncytium formation.
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b18-00714
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31061326; ● Summary page in Scopus @ Elsevier: 2-s2.0-85065672034

(DOI: 10.1248/bpb.b18-00714, PubMed: 31061326, Elsevier: Scopus) Seira Naofumi, Yanagisawa Naoki, Suganami Akiko, Takuya Honda, Wasai Makiko, Regan W John, Keijo Fukushima, Yamaguchi Naoto, Tamura Yutaka, Arai Takayoshi, Murayama Toshihiko and Hiromichi Fujino :
Anti-cancer effects of MW-03, a novel indole compound, by inducing 15-hydroxyprostaglandin dehydrogenase and cellular growth inhibition in the LS174T human colon cancer cell line,
Biological & Pharmaceutical Bulletin, 40, 10, 1806-1812, 2017.

(要約): Increases in the expression of prostaglandin E (PGE) are widely known to be involved in aberrant growth in the early stage of colon cancer development. We herein demonstrated that the novel indole compound MW-03 reduced PGE-induced cAMP formation by catalization to an inactive metabolite by inducing 15-hydroxyprostaglandin dehydrogenase through the activation of peroxisome proliferator-activated receptor-γ. MW-03 also inhibited colon cancer cell growth by arresting the cell cycle at the S phase. Although the target of MW-03 for cell cycle inhibition has not yet been identified, these dual anti-cancer effects of MW-03 itself and/or its leading compound(s) on colon cancer cells may reduce colon cancer development and, thus, have potential as a novel treatment for the early stage of this disease.
(キーワード): Antineoplastic Agents / Cell Line, Tumor / Cell Proliferation / Colonic Neoplasms / Cyclic AMP / Dinoprostone / Humans / Hydroxyprostaglandin Dehydrogenases / Indoles / PPAR gamma
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b17-00458
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28966256; ● Summary page in Scopus @ Elsevier: 2-s2.0-85030767955

(DOI: 10.1248/bpb.b17-00458, PubMed: 28966256, Elsevier: Scopus)

総説・解説: 研究者総覧に該当データはありませんでした。
講演・発表: Masaki Imanishi, Keijo Fukushima, Licht Miyamoto, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya :
The efficient anticancer therapeutic strategy targeting PARP activation,
The 25th Korea-Japan Joint Seminar, Sep. 2024. Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Mitsuhiro Goda, Naoto Okada, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa :
Development of therapeutic agents using drug discovery tools and large-scale medical information,
FIP2019, Abu Dhabi, Sep. 2019. Niimura Takahiro, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa :
Nicorandil improve prognosis of cardiac arrest patient: A large-scale medical information analysis,
FIP2019, Abu Dhabi, Sep. 2019. Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki :
Utilizing Real-World Big Data in the Search for New Renoprotective Drugs,
Joint Hypertension 2018 Scientific Sessions, Sep. 2018. Seira Naofumi, Yamagata Kazuyuki, Keijo Fukushima, Araki Yumi, Kurata Naoki, Yanagisawa Naoki, Mashimo Masato, Nakamura Hiroyuki, Regan W. John, Murayama Toshihiko and Hiromichi Fujino :
Hypoxia inducible factor-1alpha regulates human EP4 receptor expression by binding to specificity protein-1,
The 3rd Chiba University-Mahidol University Joint Symposium on Pharmaceutical Sciences, Aug. 2018. Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki :
Renoprotective effects of edoxaban, a factor Xa inhibitor,
18th World Congress of Basic and Clinical Pharmacology, Jul. 2018. Yoshito Zamami, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Toshiaki Tamaki and Keisuke Ishizawa :
Search for drugs that attenuate the anti tumor effect of bevacizumab using adverse event database,
18th World Congress of Basic and Clinical Pharmacology, Jul. 2018. Hiromichi Fujino, Araki Yumi, Suganami Akiko, Endo Suzu, Takano Harumi, Masuda Yuta, Keijo Fukushima, Regan W. John, Murayama Toshihiko and Tamura Yutaka :
PGE1 and E3 show lower efficacies than E2 to beta-catenin-mediated activity as biased ligands of EP4 prostanoid receptors,
18th World Congress of Basic and Clinical Pharmacology, Jul. 2018. 今西正樹, 福島圭穣, 近藤宏祐, 五味義輝, 亀井もえか, 松田真衣, 宮本理人, 船本雅文, 藤野裕道, 池田康将, 土屋浩一郎 :
シスプラチン前投与がメラノーマ血行性転移に与える影響の検討,
第98回日本薬理学会年会, 2025年3月. 近藤宏祐, 今西正樹, 五味義輝, 福島圭穣, 亀井もえか, 松田真衣, 宮本理人, 船本雅文, 池田康将, 土屋浩一郎 :
シスプラチン誘導性メラノーマ血行性転移促進メカニズムの検討,
第63回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2024年11月. 野島雅孝, 今西正樹, 檜垣良也, 福島圭穣, 井上貴久, 五味義輝, 宮本理人, 船本雅文, 藤野裕道, 池田康将, 土屋浩一郎 :
PRELID2の膵がん新規治療標的としての可能性の検討,
第63回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2024年11月. 植村宥香, 今西正樹, 常松保乃加, 檜垣良也, 福島圭穣, 宮本理人, 船本雅文, 堀ノ内裕也, 池田康将, 藤野裕道, 常山幸一, 土屋浩一郎 :
藍葉含有成分による肺動脈血管リモデリング形成作用，およびendothelin-1発現制御メカニズムの検討,
第63回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2024年11月. 今西正樹, 福島圭穣, 近藤宏祐, 野島雅孝, 五味義輝, 澤村貴哉, 上田恵佑, 宮本理人, 船本雅文, 藤野裕道, 池田康将, 土屋浩一郎 :
PARP活性化を標的とした効率的がん治療戦略の提案,
第63回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2024年11月. 東山晃子, 大西朗人, 柳川瞬矢, 清良尚史, Regan W John, 大川内健人, 傳田将也, 福島圭穣, 西野耕平, 大髙章, 小迫英尊, 藤野裕道 :
細胞の増殖性を調整するヒト EP4 受容体細胞内第3ループ領域を認識するキナーゼの探索,
生体機能と創薬シンポジウム2024, 2024年11月. 三竿顕也, 福島圭穣, 藤野裕道 :
内因性カンナビノイド2-arachidonoylglycerolによる新規抗結腸がん作用,
第63回日本薬学会中国四国支部学術大会, 2024年11月. 篠原万侑, 蓮岡奈苗, 縣美穂, 福島圭穣, 藤野裕道 :
PGD₂代謝物15-keto-PGD2のヒトCRTH2受容体へのバイアス作用と役割解明,
第146回日本薬理学会近畿部会, 2024年11月. 今西正樹, 福島圭穣, 後藤廣平, 山下竜介, 野島雅孝, 澤村貴哉, 上田恵佑, 中山涼, 宮本理人, 船本雅文, 藤野裕道, 池田康将, 土屋浩一郎 :
低酸素環境によるPARP活性化を介した5-FUの膵がん治療効果減弱メカニズムの解析,
第31回日本がん予防学会総会, 2024年9月. 福島圭穣, 藤野裕道 :
EP4受容体下流の大腸がん促進因子の探索,
生体機能と創薬シンポジウム2024, 2024年8月. 濵口綾花, 福田隼, 松原光太郎, 藤原広一, 渡邉瑞貴, 福島圭穣, 周東智, 藤野裕道 :
レゾルビン E シリーズとその誘導体の抗炎症作用の検討,
生体機能と創薬シンポジウム2024, 2024年8月. 植木花織, 川崎淳一郎, 吉松敬誠, 松本礼, 福島圭穣, 藤野裕道 :
histamineH1受容体の発現量とloratadineへの感受性について,
日本薬学会第144年会，横浜，2024年3月29日, 2024年3月. 東山晃子, 大西朗人, 柳川瞬矢, 清良尚史, W. John Regan, 大川内健人, 傳田将也, 福島圭穣, 西野耕平, 大髙章, 小迫英尊, 藤野裕道 :
EP4受容体の細胞内第3ループ領域に相互作用する因子の探索,
日本薬学会第144年会, 2024年3月. 安田美紀, 新居千夏, 杉下諒, 福島圭穣, 湯浅浩気, 琴浦聡, 藤野裕道 :
プラズマローゲンによるBACE1発現抑制機構の解明,
日本薬学会第144年会, 2024年3月. 今西正樹, 井上貴久, 福島圭穣, 五味義輝, 檜垣良也, 野島雅孝, 近藤宏祐, 澤村貴哉, 山下竜介, 中山涼, 常松保乃加, 後藤廣平, 宮本理人, 船本雅文, 藤野裕道, 池田康将, 土屋浩一郎 :
TCGAがんゲノムビッグデータによる膵がん悪性化因子の網羅的探索と腫瘍血管新生の寄与についての検討,
第53回日本心脈管作動物質学会年会, 2024年2月. 小西勇夢, 福島圭穣, W. John Regan, 藤野裕道 :
EP4プロスタノイド受容体下流の大腸がん原因因子の同定と誘導メカニズムの解明,
第144回日本薬理学会近畿部会，高槻, 2024年. 柳川瞬矢, 東山晃子, 福島圭穣, W. John Regan, 藤野裕道 :
ProteinkinaseAが制御するEP4受容体シグナル伝達メカニズムの解明,
第144回日本薬理学会近畿部会，高槻, 2024年. 安田美紀, 新居千夏, 杉下諒, 福島圭穣, 湯浅浩気, 琴浦聡, 藤野裕道 :
プラズマローゲンによるBACE1発現抑制機構の解明,
日本薬学会第144年会,横浜,2024年3月29日, 2024年. 東山晃子, 大西朗人, 柳川瞬矢, 清良尚史, W John Regan, 大川内健人, 傳田将也, 福島圭穣, 西野耕平, 大髙章, 小迫英尊, 藤野裕道 :
EP4受容体の細胞内第3ループ領域に相互作用する因子の探索,
日本薬学会第144年会,横浜,2024年3月29日, 2024年. 常松保乃加, 今西正樹, 植村宥香, 檜垣良也, 福島圭穣, 森崎実友, 桂明里, 宮本理人, 船本雅文, 堀ノ内裕也, 池田康将, 藤野裕道, 常山幸一, 土屋浩一郎 :
藍含有成分はendothelin-1発現を制御して肺動脈血管リモデリングを形成させる,
次世代を担う若手のための創薬・医療薬理シンポジウム2023, 2023年8月. 澤村貴哉, 今西正樹, 福島圭穣, 山下竜介, 近藤宏祐, 中山涼, 五味義輝, 常松保乃加, 井上貴久, 後藤廣平, 宮本理人, 船本雅文, 藤野裕道, 池田康将, 土屋浩一郎 :
PARP阻害剤は低酸素環境下において生じる5-FU治療効果の減弱を回復させる,
生体機能と創薬シンポジウム2023, 2023年8月. 五味義輝, 今西正樹, 井上貴久, 福島圭穣, 山下竜介, 中山涼, 野島雅孝, 近藤宏祐, 澤村貴哉, 常松保乃加, 後藤廣平, 宮本理人, 船本雅文, 藤野裕道, 池田康将, 土屋浩一郎 :
TCGAがんゲノムビッグデータとGEOトランスクリプトームデータとの統合解析による膵がん治療標的候補遺伝子の探索,
生体機能と創薬シンポジウム2023, 2023年8月. 山下真由, 山本瞳, 篠原万侑, 福島圭穣, 菅波晃子, 田村裕, 藤野裕道 :
PGJ2のヒトEP2プロスタノイド受容体を介したcAMP産生に対する影響,
日本薬学会第143年会, 2023年3月. 中野佑基, 松本聖加, 大木元綾夏, 染谷早紀, 福島圭穣, 藤野裕道 :
EP4プロスタノイド受容体シグナルの代謝機構への影響,
日本薬学会第143年会, 2023年3月. 岡林春花, 安田美紀, 新居千夏, 福島圭穣, 湯浅浩気, 琴浦聡, 藤野裕道 :
プラズマローゲンによるアルツハイマー病発症予防メカニズムの解明,
日本薬学会第143年会, 2023年3月. 縣美穂, 蓮岡奈苗, 間下雅士, 福島圭穣, 藤野裕道 :
プロスタグランジンD2代謝物のCRTH2受容体を介した機能的差異の解明,
日本薬学会第143年会, 2023年3月. 近藤宏祐, 今西正樹, 山下竜介, 福島圭穣, 中山涼, 常松保乃加, 井上貴久, 後藤廣平, 宮本理人, 船本雅文, 藤野裕道, 池田康将, 土屋浩一郎 :
5-FUの膵がん細胞増殖抑制効果に対する低酸素―PARP活性化シグナルの役割,
第262回徳島医学会学術集会(徳島), 2023年2月. 今西正樹, 山下竜介, 福島圭穣, 近藤宏祐, 中山涼, 常松保乃加, 井上貴久, 後藤廣平, 船本雅文, 藤野裕道, 池田康将, 土屋浩一郎 :
5-FU膵がん細胞増殖抑制効果に対する低酸素-PARPシグナルの役割,
第52回心脈管作動物質学会, 2023年2月. 柳川瞬矢, 大西朗人, 東山晃子, W John Regan, 福島圭穣, 藤野裕道 :
EP4プロスタノイド受容体の1アミノ酸変異によるシグナル伝達変化,
生体機能と創薬シンポジウム2023，徳島, 2023年. 三竿顕也, 福島圭穣, 藤野裕道 :
Arachidonicacidおよび2-arachidonoylglycerolによるcyclooxygenase-2分解促進作用,
生体機能と創薬シンポジウム2023，徳島, 2023年. 篠原万侑, 蓮岡奈苗, 縣美穂, 福島圭穣, 藤野裕道 :
プロスタグランジンD2代謝物のCRTH2受容体を介した機能的差異の解明,
生体機能と創薬シンポジウム2023，徳島, 2023年. 篠原万侑, 蓮岡奈苗, 縣美穂, 福島圭穣, 藤野裕道 :
プロスタグランジンD₂代謝物のCRTH2受容体を介したバイアス活性の解明,
第97回日本薬理学会年会，神戸, 2023年. 三竿顕也, 福島圭穣, 藤野裕道 :
内因性カンナビノイド2-アラキドノイルグリセロール(2-AG)の抗結腸がんメカニズムの解明,
第97回日本薬理学会年会，神戸, 2023年. 福島圭穣, 遠藤すず, 妹尾香奈穂, W John Regan, 藤野裕道 :
15-Keto-PGE2はPGE2によるシグナルを抑制するバイアスアゴニストとして作用する,
第97回日本薬理学会年会，神戸, 2023年. 濵口綾花, 福田隼, 藤原広一, 原田智史, 福島圭穣, 高栁和伸, 周東智, 藤野裕道 :
Eタイプresolvinファミリーの異なる作用は，協奏的に炎症を終息させる,
第97回日本薬理学会年会，神戸, 2023年. 福島圭穣, 藤野裕道 :
EP3プロスタノイド受容体サブタイプを高発現するヒト大腸がんクラスターの同定と性質評価,
第96回日本薬理学会年会, 2022年11月. 三竿顕也, 北島満里子, 村木拓斗, 林隼太郎, 高橋晃輝, 福島圭穣, 北井淳一郎, 奥村明子, 吉田博也, 石川勇人, 藤野裕道 :
パラグアイ原産ハーブCyclollepis genistoides D. Don(パロアッスル)の抗糖尿病生物活性成分含有画分の活性評価,
第96回日本薬理学会年会, 2022年11月. 村嶋優香, 堀ノ内裕也, 山田佑人, 吉岡駿, 福島圭穣, 久禮匠, 佐々木尚史, 藤野裕道, 四宮一昭, 池田康将 :
フィブラート系薬剤の腎保護効果に関する検討,
第61回日本薬学会中四国支部学術大会, 2022年11月. 山下竜介, 今西正樹, 福島圭穣, 近藤宏祐, 中山涼, 常松保乃加, 井上貴久, 後藤廣平, 船本雅文, 藤野裕道, 池田康将, 土屋浩一郎 :
低酸素がん微小環境におけるPARP活性化は5-FUによる膵がん細胞増殖抑制効果の減弱に寄与する,
第142回日本薬理学会近畿部会, 2022年11月. 福島圭穣, 藤野裕道 :
プロスタノイドEP2受容体とEP4受容体,
生体機能と創薬シンポジウム2022, 2022年8月. 三竿顕也, 福島圭穣, 藤野裕道 :
内因性カンナビノイドによる抗結腸がんメカニズムの解明,
第63回日本生化学会中国・四国支部例会, 2022年5月. 小林春花, 岡林春花, 安田美紀, 福島圭穣, 川村純, 琴浦聡, 藤野裕道 :
アラキドン酸による神経毒生を緩和するプラズマローゲン作用の解明,
日本薬学会第142年会，名古屋, 2022年3月. 濵口綾花, 福島圭穣, 福田隼人, 藤原広一, 周東智, 藤野裕道 :
Resolvin E-seriesの炎症収束作用の検討,
日本薬学会第142年会，名古屋, 2022年3月. 妹尾香奈穂, 山本瞳, 遠藤すず, W John Regan, 福島圭穣, 藤野裕道 :
プロスタグランジンD2の代謝物はDPプロスタノイド受容体に対してバイアスアゴニストとして働く,
第95回日本薬理学会年会，福岡, 2022年3月. 大西朗人, 東山晃子, 柳川瞬矢, 清良尚史, W John Regan, 大川内健人, 傳田将也, 福島圭穣, 大髙章, 藤野裕道 :
プロスタノイドEP4受容体の1アミノ酸変異によるシグナル伝達プロファイル変化,
第95回日本薬理学会年会，福岡, 2022年3月. 池田康将, 濱野裕章, 合田光寛, 福島圭穣, 岸誠司, 中馬真幸, 座間味義人, 宮本理人, 石澤啓介, 藤野裕道, 粟飯原賢一, 土屋浩一郎, 玉置俊晃 :
シスプラチン起因性腎障害の予防薬の探索・同定,
第94回日本薬理学会年会, 2021年3月. 蓮岡奈苗, 縣美穂, 間下雅士, 福島圭穣, 藤野裕道 :
PGD2およびその代謝物によるCRTH2受容体へのバイアス作用の解明,
日本薬学会第141年会, 2021年3月. 松本聖加, 中野佑基, 高橋弘喜, 楠屋陽子, 村山俊彦, 福島圭穣, 藤野裕道 :
PGE2による結腸がん細胞内代謝変化の解析,
日本薬学会第141年会, 2021年3月. 鷹野晴美, 妹尾香奈穂, 山下真由, 荒木祐美, W John Regan, 福島圭穣, 藤野裕道 :
EP4プロスタノイド受容体を介したプロスタグランジンD2のバイアス性による抗癌作用,
第94回日本薬理学会年会, 2021年3月. 松本礼, 植木花織, 増田雄大, 間下雅士, 福島圭穣, 藤野裕道 :
結腸癌転移に関与するヒスタミンH1受容体作用の解明,
2021年3月. 三竿顕也, 福島圭穣, 藤野裕道 :
内因性カンナビノイドによる抗結腸がんメカニズムの解明,
日本薬学会第141年会, 2021年. 池田康将, 濱野裕章, 合田光寛, 福島圭穣, 岸誠司, 石澤啓介, 土屋浩一郎, 玉置俊晃 :
シスプラチン起因性腎障害を予防する既存薬の同定,
第63回日本腎臓学会学術総会, 2020年8月. 杉山学, 大西朗人, 森崎巧也, 重永章, 福島圭穣, 大髙章, 藤野裕道 :
inteinシステムを用いたプロスタノイドEP4受容体の局在解析を目指して,
日本薬学会第140年会, 2020年3月. 山際菜月, 小林春花, 福島圭穣, 岡林春花, 川村純, 琴浦聡, 藤野裕道 :
アラキドン酸による神経毒性作用を緩和する有効な生理活性脂質としてのプラズマローゲン種の同定,
日本薬学会第140年会, 2020年3月. 北川加奈, 濱口綾花, 間下雅士, W. John Regan, 福島圭穣, 藤野裕道 :
ヒト結腸がんHCA-7細胞においてインターロイキン4はEP4プロスタノイド受容体発現を抑制する,
第93回日本薬理学会年会, 2020年3月. 遠藤すず, 妹尾香奈穂, 鷹野晴美, 荒木祐美, W. John Regan, 福島圭穣, 藤野裕道 :
PGE2代謝物 15-keto-PGE2はバイアスアゴニストとしてEP2およびEP4プロスタノイド受容体に作用する,
第93回日本薬理学会年会, 2020年3月. 濱野裕章, 池田康将, 合田光寛, 福島圭穣, 岸誠司, 武智研志, 中馬真幸, 座間味義人, 堀ノ内裕也, 宮本理人, 藤野裕道, 石澤啓介, 土屋浩一郎, 玉置俊晃 :
シスプラチン誘発性腎障害を予防する既存薬物の同定,
第260回徳島医学会学術集会(令和元年度冬期), 2020年2月. 中馬真幸, 合田光寛, 新村貴博, 座間味義人, 武智研志, 石澤有紀, 濱野裕章, 石田俊介, 新村貴博, 近藤正輝, 坂東貴司, 岡田直人, 福島圭穣, 藤野裕道, 土屋浩一郎, 堀ノ内裕也, 池田康将, 楊河宏章, 石澤啓介 :
ドラッグリポジショニング手法を用いたバンコマイシン関連腎障害の予防薬探索とその有用性の検討,
第13回日本腎臓病薬物療法学会学術集会・総会, 2019年11月. 増田雄大, 松本聖加, 松本礼, 福島圭穣, 藤野裕道 :
抗ヒスタミン薬による大腸がん誘発への有害事象の検討,
第26回日本免疫毒性学会学術年会, 2019年7月. 新村貴博, 座間味義人, 石澤有紀, 合田光寛, 武智研志, 中馬真幸, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 石澤啓介 :
大規模医療情報を用いたニコランジルの心肺停止後予後改善効果の検討,
医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, 2019年7月. 合田光寛, 斉家和仁, 前川晃子, 神田将哉, 吉田愛美, 村井陽一, 新村貴博, 石澤有紀, 座間味義人, 中馬真幸, 武智研志, 濱野裕章, 岡田直人, 福島圭穣, 藤野裕道, 土屋浩一郎, 堀ノ内裕也, 池田康将, 楊河宏章, 石澤啓介 :
医療ビッグデータを活用したシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証,
第4回中四国臨床薬理学会, 2019年7月. 新村貴博, 座間味義人, 石澤有紀, 合田光寛, 武智研志, 中馬真幸, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 石澤啓介 :
医療ビッグデータ解析と基礎研究を融合した薬剤性副作用の機序解明および治療薬の開発,
第29回日本医療薬学会年会シンポジウム13, 2019年3月. 近藤正輝, 今西正樹, 福島圭穣, 堀ノ内裕也, 石澤有紀, 石澤有紀, 合田光寛, 座間味義人, 武智研志, 中馬真幸, 池田康将, 藤野裕道, 土屋浩一郎, 石澤啓介 :
キサンチンオキシダーゼ阻害剤による新規血管線維化抑制機構の検討,
日本薬学会第139年会大学院生シンポジウムGS03, 2019年3月. 堀ノ内裕也, 池田康将, 濱野裕章, 今西正樹, 福島圭穣, 合田光寛, 武智研志, 宮本理人, 石澤有紀, 座間味義人, 藤野裕道, 石澤啓介, 土屋浩一郎, 玉置俊晃 :
慢性腎不全関連骨格筋萎縮における鉄代謝異常,
第92回日本薬理学会年会, 2019年3月. 新村貴博, 座間味義人, 石澤有紀, 齊藤広海, 今西正樹, 武智研志, 中馬真幸, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 石澤啓介 :
大規模医療情報データベースおよび遺伝子発現データベースを活用した薬剤性心筋炎に対する予防薬の探索,
第28回日本医療薬学会年会シンポジウム, 2018年11月. 堀ノ内裕也, 池田康将, 福島圭穣, 濱野裕章, 今西正樹, 石澤有紀, 座間味義人, 武智研志, 藤野裕道, 石澤啓介, 土屋浩一郎, 玉置俊晃 :
リアルワールドビッグデータを活用した新規腎保護薬の探索,
第28回日本医療薬学会年会, 2018年11月. 堀ノ内裕也, 池田康将, 濱野裕章, 今西正樹, 福島圭穣, 合田光寛, 武智研志, 宮本理人, 石澤有紀, 座間味義人, 藤野裕道, 石澤啓介, 土屋浩一郎, 玉置俊晃 :
慢性腎不全関連サルコペニアにおける鉄の関与,
第134回日本薬理学会近畿部会, 2018年11月. 生藤来希, 今西正樹, 山川祐介, 福島圭穣, 前川晃子, 堀ノ内裕也, 石澤有紀, 合田光寛, 座間味義人, 武智研志, 中馬真幸, 池田康将, 藤野裕道, 土屋浩一郎 :
大腸がん増大におけるがん関連線維芽細胞由来ERKSの役割,
第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2018年11月. 堀ノ内裕也, 池田康将, 福島圭穣, 石澤有紀, 藤野裕道, 玉置俊晃 :
リアルワールドデータを活用した新規腎保護薬の探索,
第48回日本腎臓学会西部学術大会, 2018年9月. 新村貴博, 座間味義人, 石澤有紀, 合田光寛, 今西正樹, 武智研志, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 石澤啓介 :
大規模医療情報を活用した新規心肺蘇生後脳症治療薬の探索,
第29回霧島神経薬理フォーラム, 2018年8月. 今西正樹, 近藤正輝, 山川裕介, 生藤来希, 村井陽一, 座間味義人, 武智研志, 中馬真幸, 堀ノ内裕也, 福島圭穣, 石澤有紀, 池田康将, 藤野裕道, 土屋浩一郎, 石澤啓介 :
Angiotensin II誘発性心臓線維化は線維芽細胞特異的ERK5欠損マウスにおいて亢進される,
第133回日本薬理学会近畿部会, 2018年6月. 座間味義人, 三井茉綸, 石澤有紀, 武智研志, 今西正樹, 堀ノ内裕也, 福島圭穣, 池田康将, 藤野裕道, 土屋浩一郎, 玉置俊晃, 石澤啓介 :
有害事象自発報告データベースを活用したベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究,
日本薬学会第138年会, 2018年3月. 新村貴博, 座間味義人, 石澤有紀, 今西正樹, 武智研志, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 玉置俊晃, 石澤啓介 :
ドラッグリポジショニング手法を用いた心肺蘇生後脳症治療薬の探索,
日本薬学会第138年会, 2018年3月. 渡嘉敷夏海, 倉田直希, 三竿顕也, 荒木祐美, 清良尚史, 山際菜月, 杉山学, 福島圭穣, W John REGAN, 村山俊彦, 藤野裕道 :
ヒト結腸がんHCA-7 細胞における酪酸によるEP4 受容体発現系への影響,
日本薬学会第138年会, 2018年3月. 福島圭穣, 市川和哉, 上野崇宏, 稲垣孝行, 宮川泰宏, 千﨑康司, 藤野裕道, 山田清文 :
関節リウマチ治療薬を対象とした有害事象自発報告データベースFAERSを用いた感染症リスクの比較,
第256回徳島医学会学術集会, 2018年2月. 堀ノ内裕也, 池田康将, 福島圭穣, 濱野裕章, 今西正樹, 石澤有紀, 座間味義人, 藤野裕道, 石澤啓介, 土屋浩一郎, 玉置俊晃 :
大規模医療情報データベース解析と基礎研究の融合による新規腎保護薬の探索,
第256回徳島医学会学術集会(平成29年度冬期), 2018年2月. 新村貴博, 座間味義人, 石澤有紀, 今西正樹, 武智研志, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 玉置俊晃, 石澤啓介 :
大規模医療情報を活用した心肺停止患者に対するニコランジルの有効性に関する検討,
第256回徳島医学会学術集会(平成29年度冬期), 2018年2月. 堀ノ内裕也, 池田康将, 福島圭穣, 今西正樹, 石澤有紀, 座間味義人, 藤野裕道, 石澤啓介, 土屋浩一郎, 玉置俊晃 :
第Xa因子阻害剤の腎保護効果,
第47回日本心脈管作動物質学会, 2018年2月. 堀ノ内裕也, 池田康将, 福島圭穣, 石澤有紀, 藤野裕道, 玉置俊晃 :
医療ビッグデータを活用した腎保護薬の探索,
2017年度肥満・糖尿病クラスター・ミニリトリート, 2018年2月. 堀ノ内裕也, 池田康将, 福島圭穣, 今西正樹, 石澤有紀, 座間味義人, 藤野裕道, 石澤啓介, 土屋浩一郎, 玉置俊晃 :
第Xa因子阻害薬の腎保護効果,
第10回心・血管クラスター・ミニリトリート, 2017年. 新村貴博, 座間味義人, 石澤有紀, 今西正樹, 武智研志, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 玉置俊晃, 石澤啓介 :
大規模医療情報を用いて新規心肺蘇生後症候群治療薬の開発を志向したドラッグリポジショニング研究,
第38回日本臨床薬理学会学術総会, 2017年12月. 三井茉綸, 座間味義人, 石澤有紀, 新村貴博, 武智研志, 今西正樹, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 玉置俊晃, 石澤啓介 :
有害事象自発報告データベースを基にしたベバシズマブと相互作用を起こす薬剤の探索研究,
第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2017年10月. 新村貴博, 座間味義人, 石澤有紀, 今西正樹, 武智研志, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 玉置俊晃, 石澤啓介 :
心肺停止患者の予後に与えるニコランジルの影響-大規模レセプト情報を用いた検討,
第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2017年10月. 漆崎汐里, 座間味義人, 石澤有紀, 新村貴博, 武智研志, 今西正樹, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 玉置俊晃, 石澤啓介 :
大規模医療情報を活用して新規心肺蘇生後症候群治療薬の開発を志向したドラッグリポジショニング研究,
第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2017年10月. 荒木祐美, 菅波晃子, 遠藤すず, 水口博之, 福島圭穣, W John REGAN, 村山俊彦, 田村裕, 藤野裕道 :
PGE1とPGE3のバイアス性と癌抑制機構の解明,
第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 2017年10月. 新村貴博, 座間味義人, 石澤有紀, 今西正樹, 武智研志, 福島圭穣, 堀ノ内裕也, 池田康将, 藤野裕道, 土屋浩一郎, 玉置俊晃, 石澤啓介 :
心肺蘇生後症候群治療薬の開発を目的としたドラッグリポジショニング研究-大規模医療情報を活用した検討-,
第255回徳島医学会学術集会, 2017年8月.

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補助金・競争的資金: single cell統合解析により得られたEP4プロスタノイド受容体発現大腸がん細胞の解析 (研究課題/領域番号: 25K10002 )
プロスタノイドEP4受容体高発現大腸がんの治療的探索を目指した機能解析 (研究課題/領域番号: 22K15293 )
プロスタノイド受容体サブタイプの転換と大腸がん発生・悪性化メカニズムの解明 (研究課題/領域番号: 19K16374 )
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2026年3月21日更新

研究者番号: 10805112

所属（現在）: 2025/4/1 : 徳島大学, 大学院医歯薬学研究部(薬学域), 准教授

所属（過去の研究課題 情報に基づく）*注記: 2019/4/1 – 2025/4/1 : 徳島大学, 大学院医歯薬学研究部(薬学域), 助教

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小区分47040:薬理学関連

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薬理学 / プロスタノイド受容体 / 大腸がん / バイオインフォマティクス / プロスタグランジンE2 / EP4受容体 / EP3受容体 / プロスタノイド / EP受容体 / 薬学 / Gタンパク質共役受容体 / Gタンパク質共役型受容体 / プロスタグランジン受容体

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