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安部秀斉

徳島大学

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2023年3月22日更新

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学歴: 2001/3: 京都大学大学院医学研究科修了(医博修了)
学位: 博士(医学) (京都大学) (2001年3月)
職歴・経歴: 2005/4: 徳島大学非常勤講師, 医学部 (-2008.3.)
2008/4: 徳島大学講師, 病院 (-2008.12.)
2008/4: 徳島大学講師, 医学部 (-2009.3.)
2009/1: 徳島大学講師, 病院 (-2009.6.)
2009/6: 徳島大学准教授, 大学院ヘルスバイオサイエンス研究部 (-2015.3.)
2015/4: 徳島大学准教授, 大学院医歯薬学研究部 (-2021.2.)

専門分野・研究分野: 腎臓学 (Nephrology)

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2023年3月22日更新

専門分野・研究分野: 腎臓学 (Nephrology)
担当経験のある授業科目: 研究者総覧に該当データはありませんでした。
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2023年3月22日更新

専門分野・研究分野: 腎臓学 (Nephrology)

研究テーマ: 腎不全の修復・再生に関する研究, 糖尿病性腎症の分子病態に関する研究

著書

安部秀斉 :
AI時代の糖尿病性腎臓病の特異的バイオマーカー -限界と挑戦-,
北隆館, 東京, 2019年9月. 安部秀斉 :
糖尿病性腎症の分子病態解明と修復治療法の開発,
2019年3月. 安部秀斉 :
AI時代のhybrid型医工アプローチによるアンチエイジング,
北隆館, 2019年. 安部秀斉 :
AI時代の病態特異的バイオマーカー -限界と挑戦,
北隆館, 2019年. 安部秀斉 :
Pandemicな慢性腎臓病に対する移植医療の現状と未来像,
北隆館, 2019年. 安部秀斉 :
新たな国民病，慢性腎臓病CKD,
2013年10月.

(徳島大学機関リポジトリ): ● Metadata: 112651

(徳島大学機関リポジトリ: 112651) Tatsuya Tominaga, Hideharu Abe, Akira Mima, Kojiro Nagai, Matsubara Takeshi and Toshio Doi :
Role of Smad 1 Signaling in Pathogenesis of Diabetic Nephropathy,
Nova Science Publishers, Sep. 2012. 安部秀斉 :
糖尿病性腎症の病態と診断,
日本臨床, 東京都, 2012年7月. 安部秀斉 :
急性・慢性腎不全,
西村書店, 東京都, 2012年7月. 安部秀斉 :
CKD,
2012年7月. 安部秀斉 :
腎疾患の病態形成におけるBMP4・Smad1の役割,
株式会社中外医学社, 東京, 2011年. 安部秀斉 :
CKD(慢性腎臓病)の実際∼治療の考え方∼,
阿南医師会中央病院, 徳島, 2010年5月. 安部秀斉 :
ネフローゼ症候群の現状と今後の治療戦略,
株式会社東京医学社, 東京, 2010年3月.

論文

Masanori Minato, Taichi Murakami, Naoki Takahashi, Hiroyuki Ono, Kenji Nishimura, Masanori Tamaki, Kojiro Nagai, Hideharu Abe, Masayuki Iwano, Kensuke Joh and Toshio Doi :
Glucocorticoid-dependent Tubulointerstitial Nephritis with IgM-positive Plasma Cells Presenting with Intracellular Crystalline Inclusions within the Rough Endoplasmic Reticulum.,
Internal Medicine, 2021.

(要約): Tubulointerstitial nephritis (TIN) with IgM-positive plasma cells (IgMPC-TIN) is an autoimmune kidney disease characterized by IgM/CD138-double-positive plasma cell infiltration in the tubulointerstitium. A 50-year-old man developed IgMPC-TIN and presented with crystalline inclusions in the rough endoplasmic reticulum. Intracellular crystal formation is a rare finding in paraprotein-related kidney diseases, but this case showed no pathogenic monoclonal immunoglobulin. Prednisolone (PSL, 30 mg) improved the TIN, but PSL tapering resulted in the recurrence of TIN. Combination therapy with 15 mg PSL and 150 mg mizoribine ultimately stabilized TIN. This case offers original evidence concerning the pathophysiology and treatment strategy of IgMPC-TIN.
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.7118-21
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33840699; ● Search Scopus @ Elsevier (PMID): 33840699; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.7118-21

(DOI: 10.2169/internalmedicine.7118-21, PubMed: 33840699) Taichi Murakami, Kenji Nishimura, Hiroyuki Ono, Sayo Ueta, Eriko Shibata, Seiji Kishi, Masanori Tamaki, Keiko Miya, Hisato Shima, Manabu Tashiro, Tomoko Inoue, Kazuhiko Kawahara, Kojiro Nagai, Hideharu Abe, Jun Minakuchi and Toshio Doi :
Clinical characteristics associated with 1-year tolvaptan efficacy in autosomal dominant polycystic kidney disease with a wide range of kidney functions.,
The Journal of Medical Investigation : JMI, Vol.67, No.3.4, 315-320, 2020.

(要約): Autosomal dominant polycystic kidney disease (ADPKD) develops into end-stage kidney disease by 65 years of age in an estimated 45%-70% of patients. Recent trials revealed that tolvaptan inhibits disease progression both in early-stage or late-stage ADPKD ; however, stratified analysis showed a difference of favorable factors correlated with tolvaptan efficacy between early-stage and late-stage ADPKD. Thus, we examined the efficacy of tolvaptan in ADPKD with a wide range of estimated glomerular filtration rates (eGFR). We enrolled 24 patients with eGFR 35.3 (28.0-65.5) ml / min / 1.73m2 and evaluated treatment effect as ΔΔeGFR (ml / min / 1.73m2 / year) or ΔΔtotal kidney volume (TKV) (% / year) that was calculated as post-treatment annual change - pre-treatment annual change. Pre ΔeGFR was significantly low in eGFR responders, defined as ΔΔeGFR > 0 ml / min / 1.73m2 / year. In eGFR responders, pre ΔeGFR, post ΔeGFR, eGFR, TKV, and proteinuria were significantly correlated with ΔΔeGFR. In TKV responders defined as ΔΔTKV > 5 % / year, we identified hypertension history, proteinuria, TKV, and post ΔTKV as significantly correlated factors with ΔΔTKV. In conclusion, pre ΔeGFR may be a predictive factor of therapeutic efficacy on kidney function. Tolvaptan may have greater efficacy in early-stage ADPKD with rapid GFR decline or with well-controlled blood pressure. J. Med. Invest. 67 : 315-320, August, 2020.
(徳島大学機関リポジトリ): ● Metadata: 115436
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.67.315
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33148908; ● Summary page in Scopus @ Elsevier: 2-s2.0-85095569571

(徳島大学機関リポジトリ: 115436, DOI: 10.2152/jmi.67.315, PubMed: 33148908, Elsevier: Scopus) Kenji Nishimura, Taichi Murakami, Toshihiro Sakurai, Masashi Miyoshi, Kiyoe Kurahashi, Seiji Kishi, Masanori Tamaki, Tatsuya Tominaga, Sumiko Yoshida, Kojiro Nagai, Hideharu Abe, Shu-Ping Hui, Kazuhiko Kotani and Toshio Doi :
Circulating Apolipoprotein L1 is associated with insulin resistance-induced abnormal lipid metabolism.,
Scientific Reports, Vol.9, No.1, 14869, 2019.

(要約): Circulating ApolipoproteinL1 (ApoL1) is a component of pre-β-high-density lipoprotein (HDL), however little is known about the relationship of ApoL1 with cardiometabolic factors. Considering previous studies reporting the correlation of ApoL1 to triglyceride, we have hypothesized that ApoL1 associates with insulin-related metabolism. The current study examined their associations in 126 non-diabetic subjects and 36 patients with type 2 diabetes (T2DM). Non-diabetic subjects demonstrated triglyceride (standardized coefficients [s.c.] = 0.204, p < 0.05), body mass index (s.c. =0.232, p < 0.05) and HDL cholesterol (s.c. = -0.203, p < 0.05) as independent determinant of ApoL1 levels, and the significant elevation of ApoL1 in metabolic syndrome. Lipoprotein fractionation analysis revealed the predominant distribution of ApoL1 in large HDL fraction, and the significant increase of ApoL1 in large LDL fraction in high ApoL1 samples with insulin resistance. In T2DM, ApoL1 was higher in T2DM with metabolic syndrome, however ApoL1 was lower with β cell dysfunction. Insulin significantly promotes ApoL1 synthesis and secretion in HepG2 cells. In conclusion, circulating ApoL1 may be associated with abnormal HDL metabolism in insulin resistant status. This may suggest a regulation of insulin signal on the ApoL1 level, leading to offer a novel insight to the ApoL1 biology.
(徳島大学機関リポジトリ): ● Metadata: 114663
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-019-51367-7
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31619724; ● Search Scopus @ Elsevier (PMID): 31619724; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-019-51367-7

(徳島大学機関リポジトリ: 114663, DOI: 10.1038/s41598-019-51367-7, PubMed: 31619724) Akiko Sakurai, Hiroyuki Ono, Arisa Ochi, Motokazu Matsuura, Sakiya Yoshimoto, Seiji Kishi, Taichi Murakami, Tatsuya Tominaga, Kojiro Nagai, Hideharu Abe and Toshio Doi :
Involvement of Elf3 on Smad3 activation-dependent injuries in podocytes and excretion of urinary exosome in diabetic nephropathy.,
PLoS ONE, Vol.14, No.5, 2019.

(要約): Diabetic nephropathy (DN) is among the most serious complications of diabetes mellitus, and often leads to end-stage renal disease ultimately requiring dialysis or renal transplantation. The loss of podocytes has been reported to have a role in the onset and progression of DN. Here, we addressed the activation mechanism of Smad3 signaling in podocytes. Expression of RII and activation of Smad3 were induced by AGE exposure (P<0.05). Reduction of the activation of RII-Smad3 signaling ameliorated podocyte injuries in Smad3-knockout diabetic mice. The bone morphogenetic protein 4 (BMP4) significantly regulated activation of RII-Smad3 signalings (P<0.05). Moreover, the epithelium-specific transcription factor, Elf3was induced by AGE stimulation and, subsequently, upregulated RII expression in cultured podocytes. Induction of Elf3 and activation of RII-Smad3 signaling, leading to a decrease in WT1 expression, were observed in podocytes in diabetic human kidneys. Moreover, AGE treatment induced the secretion of Elf3-containing exosomes from cultured podocytes, which was dependent on the activation of the TGF-β-Smad3 signaling pathway. In addition, exosomal Elf3 protein in urine could be measured only in urinary exosomes from patients with DN. The appearance of urinary exosomal Elf3 protein in patients with DN suggested the existence of irreversible injuries in podocytes. The rate of decline in the estimated Glomerular Filtration Rate (eGFR) after measurement of urinary exosomal Elf3 protein levels in patients with DN (R2 = 0.7259) might be useful as an early non-invasive marker for podocyte injuries in DN.
(徳島大学機関リポジトリ): ● Metadata: 114344
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0216788
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31150422; ● Search Scopus @ Elsevier (PMID): 31150422; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0216788

(徳島大学機関リポジトリ: 114344, DOI: 10.1371/journal.pone.0216788, PubMed: 31150422) 藤田結衣, 冨永辰也, 寒川裕未, 長井幸二郎, 安部秀斉, 土井俊夫 :
BMP4 regulates both podocyte injury and mesangial expansion in the diabetic nephropathy,
四国医学雑誌, Vol.75, No.1-2, 55-62, 2019年.

(要約): Podocyte injury and loss have been indicated as constituting the crucial pathogenesis of glomerular injury ; however, it remains necessary to elucidate the detailed molecular mechanisms and cell-to-cell response because multiple factors may cause podocyte injury. In the glomerulus, three kinds of cells (endothelial, mesangial, and parietal epithelial) react to podocyte injury. Endothelial and mesangial cells are connected with podocyte cells across the glomerular basement membrane. However, the detailed mechanisms regarding the interaction of the mesangium and podocyte injury are unclear. Diabetic nephropathy is characterized by mesangial matrix expansion caused by an excessive deposition of extracellular matrix proteins in the mesangial area, which can be observed through the increased expression of type IV collagen. We have shown that bone morphogenetic protein 4 (BMP4) signaling leads to the glomerular changes characteristic of this disorder. To analyze the effect of BMP4 was investigated in vitro and in vivo using streptozotocin (STZ)-induced and Bmp4 heterozygous knockout (Bmp4+/-) diabetic mice or podocyte-specific Bmp4 knockout mice, and Bmp4-induced or podocyte-specific transgenic mice. BMP4 positive area and mesangial area fraction showed positively correlation. Furthermore, mesangial area fraction was significantly and negatively correlated with,WT1-positive cell number, and nephrin-positive area. We also demonstrated that the induction of podocyte apoptosis by BMP4 may be mediated by p38 activation and that of caspase 3 through cleavage. In mesangial cells, BMP4 stimulation also induced phosphorylation of p38 and Smad1 and increased cleaved caspase 3, with similar significant inhibition of Smad1 activation and decreased cleaved caspase 3 mediated by dorsomorphin. These data suggest that the BMP4 signaling pathway plays important roles for the development of both podocyte injury and mesangial expansion in diabetic nephropathy.
(キーワード): BMP4 / diabetic nephropathy / podocyte / apotosis / mesangial expansion
(徳島大学機関リポジトリ): ● Metadata: 113757
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050564288726855552

(徳島大学機関リポジトリ: 113757, CiNii: 1050564288726855552) Taichi Murakami, Masanori Tamaki, Seiji Kishi, Kojiro Nagai, Hideharu Abe, Yoshimi Bando, Yuko Toyoda, Hirokazu Ogino, Yasuhiko Nishioka, Sayo Ueda, Toshio Doi and Motokazu Matsuura :
Systemic Sarcoidosis Presenting with Renal Involvement Caused by Various Sarcoidosis-associated Pathophysiological Conditions,
Internal Medicine, Vol.58, No.5, 679-684, 2019.

(要約): A 61-year-old man was diagnosed with sarcoidosis involving the lungs, eyes, parotid gland and extrathoracic lymph nodes complicated by chronic kidney injury and hypercalcemia. Kidney biopsy showed non-specific interstitial nephritis and nephrosclerosis. However, immunohistochemical staining of cell surface markers revealed a multinucleated giant macrophage surrounded by T-cells, suggesting granulomatous interstitial nephritis. Corticosteroid improved the kidney function, and reduced the serum levels of calcium and angiotensin-converting enzyme. Sarcoid nephropathy may be caused by the combination of several sarcoidosis-associated pathophysiological conditions and a comprehensive kidney examination should be performed to assess the type of injury when determining a treatment strategy.
(キーワード): Biomarkers / Biopsy / カルシウム (calcium) / Glucocorticoids / Humans / Hypercalcemia / Kidney / 男性 (male) / Middle Aged / Nephritis, Interstitial / Nephrosclerosis / Peptidyl-Dipeptidase A / Radionuclide Imaging / Sarcoidosis
(徳島大学機関リポジトリ): ● Metadata: 114405
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.1558-18
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30449791; ● Summary page in Scopus @ Elsevier: 2-s2.0-85062415769

(徳島大学機関リポジトリ: 114405, DOI: 10.2169/internalmedicine.1558-18, PubMed: 30449791, Elsevier: Scopus) Fumiaki Obata, Hideharu Abe, Taichi Murakami, Sayo Ueda, Taizo Inagaki, Masanori Minato, Hiroyuki Ono, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Fumi Kishi, Seiji Kishi, Kojiro Nagai and Toshio Doi :
Direct oral anticoagulant successfully used to treat an adult nephrotic patient complicated with portal vein thrombosis.,
CEN Case Reports, Vol.8, No.2, 134-138, 2019.

(要約): Thromboembolism is a major complication of nephrotic syndrome, with the renal vein being the most frequent site. However, the incidence of portal vein thrombosis (PVT) in patients with nephrotic syndrome is rare. We report a case of a relapsed steroid-dependent minimal change disease with incidental PVT. A 38-year-old man presented with anasarca. Elevated liver enzymes were discovered during routine blood testing within days after commencing treatment. Although drug-induced liver injuries are frequently observed with mild aminotransferase abnormality during therapy with steroid or immune-suppressive agents, imaging revealed a massive thrombus of the portal vein, which was treated by anticoagulant therapy with edoxaban. Treatment with anticoagulant therapy could normalize liver function. Two months after the initiation of treatment with edoxaban, the follow-up CT scan and ultrasound showed the disappearance of PVT. Our case suggests that much attention should be paid to PVT as a cause of liver enzyme elevation when treating patients with nephrotic syndrome.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s13730-019-00381-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30721455; ● Search Scopus @ Elsevier (PMID): 30721455; ● Search Scopus @ Elsevier (DOI): 10.1007/s13730-019-00381-9

(DOI: 10.1007/s13730-019-00381-9, PubMed: 30721455) Hideharu Abe and Toshio Doi :
A New Insight into Molecular Function of Smads Signalings in Diabetic Nephropathy.,
Advanced Techniques in Biology & Medicine, Vol.7, No.1, 2019.

(出版サイトへのリンク): ● Publication site (DOI): 10.4172/2379-1764.1000265
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.4172/2379-1764.1000265

(DOI: 10.4172/2379-1764.1000265) Masanori Tamaki, Tatsuya Tominaga, Yui Fujita, Yasuhiko Koezuka, Go Ichien, Taichi Murakami, Seiji Kishi, Keiichi Yamamoto, Hideharu Abe, Kojiro Nagai and Toshio Doi :
All-trans retinoic acid suppresses bone morphogenetic protein 4 in mouse diabetic nephropathy through a unique retinoic acid response element.,
American Journal of Physiology, Endocrinology and Metabolism, Vol.316, No.3, E418-E431, 2019.

(要約): Diabetic nephropathy (DN) causes mesangial matrix expansion, which results in glomerulosclerosis and renal failure. Collagen IV (COL4) is a major component of the mesangial matrix that is positively regulated by bone morphogenetic protein 4 (BMP4)/suppressor of mothers against decapentaplegic (Smad1) signaling. Because previous studies showed that retinoids treatment had a beneficial effect on kidney disease, we investigated the therapeutic potential of retinoids in DN, focusing especially on the regulatory mechanism of BMP4. Diabetes was induced with streptozotocin in 12-wk-old male Crl:CD1(ICR) mice, and, 1 mo later, we initiated intraperitoneal injection of all-trans retinoic acid (ATRA) three times weekly. Glomerular matrix expansion, which was associated with increased BMP4, phosphorylated Smad1, and COL4 expression, worsened in diabetic mice at 24 wk of age. ATRA administration alleviated DN and downregulated BMP4, phosopho-Smad1, and COL4. In cultured mouse mesangial cells, treatment with ATRA or a retinoic acid receptor-α (RARα) agonist significantly decreased BMP4 and COL4 expression. Genomic analysis suggested two putative retinoic acid response elements (RAREs) for the mouse Bmp4 gene. Chromatin immunoprecipitation analysis and reporter assays indicated a putative RARE of the Bmp4 gene, located 11,488-11,501 bp upstream of exon 1A and bound to RARα and retinoid X receptor (RXR), which suppressed BMP4 expression after ATRA addition. ATRA suppressed BMP4 via binding of a RARα/RXR heterodimer to a unique RARE, alleviating glomerular matrix expansion in diabetic mice. These findings provide a novel regulatory mechanism for treatment of DN.
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajpendo.00218.2018
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30601699; ● Search Scopus @ Elsevier (PMID): 30601699; ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00218.2018

(DOI: 10.1152/ajpendo.00218.2018, PubMed: 30601699) Eriko Shibata, Kojiro Nagai, Sayo Ueda, Hiroyuki Ono, Kenji Nishimura, Taizo Inagaki, Masanori Minato, Fumi Kishi, Masanori Tamaki, Taichi Murakami, Seiji Kishi, Hideharu Abe, Narushi Yokota, Jun Minakuchi and Toshio Doi :
The utility and limitation of inferior vena cava diameter as a dry weight marker.,
The Journal of Medical Investigation : JMI, Vol.66, No.1.2, 172-177, 2019.

(要約): IVCdexp was a rough marker to estimate volume status and only useful in suggesting apparent hypervolemia or hypovolemia. We should know that the IVCdexp value is affected by a lotof factors and not a definitive marker for estimating practical DW. J. Med. Invest. 66 : 172-177, February, 2019.
(徳島大学機関リポジトリ): ● Metadata: 113414
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.66.172
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31064933; ● Search Scopus @ Elsevier (PMID): 31064933; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.66.172

(徳島大学機関リポジトリ: 113414, DOI: 10.2152/jmi.66.172, PubMed: 31064933) Hideharu Abe, Akiko Sakurai and Arisa Ochi :
Induction of steady-state glomeruloid sphere by self-assembly from human embryonic kidney cells.,
Biochemical and Biophysical Research Communications, Vol.508, No.2, 654-659, 2018.

(要約): The glomerulus is a network of capillaries known as a tuft, located at the beginning of a nephron in the kidney. Here we describe a novel method for the induction of a macroscopically visible three-dimensional glomerulus-like sphere (GLS). This procedure did not require any additional cytokines and completed the formation of spheres within 24 h. After the formation was complete, GLS maintained a steady state for at least five days without proliferation and without a decrease in viability. Therefore, this procedure assists various assays for a prolong period of time. Overall, our protocol allows for a very simple mixing of cells from different sources to obtain fine-grained and highly dispersed GLSs. The kidney filtration barrier is a unique structure characterized by a complex three-dimensional framework of podocytes and endothelial cells. GLS exhibited the induction of many podocyte-specific gene profiles similar to those in adult human kidneys, suggesting that the sphere formation process is important for the maturation of podocytes. Focal segmental glomerulosclerosis (FSGS) is one of the major causes of steroid-resistant nephrotic syndrome, and some circulating permeability factors in the patient's serum FSGS have been implicated in the pathogenesis of the disease. Serum from patients with FSGS induced the collapse of GLS, which imitates the appearance of glomerulosclerosis in patients. In conclusion, the investigation and use of GLS may provide a novel method to elucidate the molecular mechanisms underlying complicated and unexplained events in glomeruli in a similar condition in adult kidneys.
(キーワード): Cells, Cultured / Glomerulosclerosis, Focal Segmental / Humans / Kidney Glomerulus
(徳島大学機関リポジトリ): ● Metadata: 115014
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2018.11.160
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30522864; ● Search Scopus @ Elsevier (PMID): 30522864; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2018.11.160

(徳島大学機関リポジトリ: 115014, DOI: 10.1016/j.bbrc.2018.11.160, PubMed: 30522864) Yui Fujita, Tatsuya Tominaga, Hideharu Abe, Yumi Kangawa, Naoshi Fukushima, Otoya Ueda, Kou-Ichi Jishage, Seiji Kishi, Taichi Murakami, Yumiko Saga, S Yashpal Kanwar, Kojiro Nagai and Toshio Doi :
An adjustment in BMP4 function represents a treatment for diabetic nephropathy and podocyte injury.,
Scientific Reports, Vol.8, No.1, 2018.

(要約): Podocyte injury has been proposed to play an important role in diabetic nephropathy; however, its pathological mechanism remains unclear. We have shown that bone morphogenetic protein 4 (BMP4) signaling leads to the glomerular changes characteristic of this disorder. To analyze the molecular mechanism of podocyte injury, the effect of BMP4 was investigated using streptozotocin (STZ)-induced, Bmp4 heterozygous knockout (Bmp4+/-) and podocyte-specific Bmp4 knockout mice. Mice with STZ-induced diabetes exhibited glomerular matrix hyperplasia and decreased numbers of podocyte nucleus-specific WT1-positive cells. The number of podocytes and proteinuria were improved in both diabetic Bmp4 knockout mouse models compared to the effects observed in the control mice. The effect of BMP4 overexpression on Bmp4-induced or podocyte-specific transgenic mice was examined. Tamoxifen-induced Bmp4-overexpressing mice exhibited mesangial matrix expansion and decreased numbers of WT1-positive cells. Podocyte-specific Bmp4-overexpressing mice displayed increased kidney BMP4 expression and mesangial matrix expansion but decreased nephrin expression and numbers of WT1-positive cells. Both lines of Bmp4-overexpressing mice exhibited increased albuminuria. In cultured podocytes, BMP4 increased phospho-p38 levels. BMP4 decreased nephrin expression but increased cleaved caspase-3 levels. p38 suppression inhibited caspase-3 activation. Apoptosis was confirmed in STZ-diabetic glomeruli and Bmp4-overexpressing mice. Bmp4 +/- mice with diabetes displayed reduced apoptosis. Based on these data, the BMP4 signaling pathway plays important roles in the development of both podocyte injury and mesangial matrix expansion in diabetic nephropathy.
(徳島大学機関リポジトリ): ● Metadata: 112896
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-018-31464-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30158674; ● Search Scopus @ Elsevier (PMID): 30158674; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-018-31464-9

(徳島大学機関リポジトリ: 112896, DOI: 10.1038/s41598-018-31464-9, PubMed: 30158674) Hideharu Abe, Akiko Sakurai, Hiroyuki Ono, Sanae Hayashi, Sakiya Yoshimoto, Arisa Ochi, Sayo Ueda, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Fumi Kishi, Seiji Kishi, Taichi Murakami, Kojiro Nagai and Toshio Doi :
Urinary Exosomal mRNA of WT1 as Diagnostic and Prognostic Biomarker for Diabetic Nephropathy,
The Journal of Medical Investigation : JMI, Vol.65, No.3.4, 208-215, 2018.

(要約): Diabetic nephropathy (DN) is the major cause of end-stage renal failure and is associated with increased morbidity and mortality as compared to other causes of renal disease. Albuminuria is often the first clinical indicator of the presence of DN. However, albuminuria or proteinuria is a common symptom in patients with various renal disorders. Therefore, specific biomarkers for the diagnosis of DN are required. A primary hallmark of DN is the progressive damage and death of glomerular podocytes, resulting in the leaking of proteins into the urine. Urinary exosomes released by podocytes are microvesicles containing information of the originated cells. Podocyte-derived signal transduction factors (PDSTFs) are good candidates to assess podocyte injuries. The profile of PDSTFs in urinary exosomes from patients with DN is different from that from patients with minimal change nehrotic syndrome. In addition, PDSTFs molecules in exosomes were derived from primary murine podocytes under high glucose conditions. Among PDSTFs in urinary exosomes, Wilms tumor 1 (WT1) levels reflected damage of diabetic glomeruli in the patients. Urinary exosomal WT1 can predict the decline in eGFR for the following several years. In conclusion, urinary exosomal WT1 is a useful biomarker to improve risk stratification in patients with DN. J. Med. Invest. 65:208-215, August, 2018.
(キーワード): Adolescent / Adult / Biomarkers / Case-Control Studies / Cells, Cultured / Diabetic Nephropathies / Exosomes / Genes, Wilms Tumor / Genetic Markers / Humans / Middle Aged / Nephrosis, Lipoid / Podocytes / Prognosis / RNA, Messenger / WT1 Proteins / Young Adult
(徳島大学機関リポジトリ): ● Metadata: 112239
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.65.208
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30282862; ● Summary page in Scopus @ Elsevier: 2-s2.0-85054429444

(徳島大学機関リポジトリ: 112239, DOI: 10.2152/jmi.65.208, PubMed: 30282862, Elsevier: Scopus) Hiroyuki Ono, Hideharu Abe, Akiko Sakurai, Arisa Ochi, Tatsuya Tominaga, Masanori Tamaki, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Masayuki Kohashi and Toshio Doi :
Novel Interplay Between Smad1 and Smad3 Phosphorylation via AGE Regulates the Progression of Diabetic Nephropathy.,
Scientific Reports, Vol.8, No.1, 2018.

(要約): ; db/db mice and probucol-treated db/db mice, which was consistent with the attenuation of ECM overproduction. These results indicate that Smad3 expression and activation or probucol treatment alters Smad1 phosphorylation, thus suggesting new molecular mechanisms underlying DN development and progression.
(徳島大学機関リポジトリ): ● Metadata: 112878
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-018-28439-1
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30002389; ● Search Scopus @ Elsevier (PMID): 30002389; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-018-28439-1

(徳島大学機関リポジトリ: 112878, DOI: 10.1038/s41598-018-28439-1, PubMed: 30002389) Seiji Kishi, 小幡史明, Hirokazu Miki, Motokazu Matsuura, Masanori Tamaki, Fumi Kishi, 西村賢二, Taichi Murakami, Hideharu Abe, Kojiro Nagai, Masahiro Abe and Toshio Doi :
A case of Lambda Light Chain Noncrystalline Proximal Tubulopathy with IgD lambda myeloma,
Internal Medicine, 2018.

(徳島大学機関リポジトリ): ● Metadata: 114401
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.1323-18
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30101939; ● Search Scopus @ Elsevier (PMID): 30101939; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.1323-18

(徳島大学機関リポジトリ: 114401, DOI: 10.2169/internalmedicine.1323-18, PubMed: 30101939) Seiji Kishi, Masanori Minato, Atsuro Saijo, Naoka Murakami, Masanori Tamaki, Motokazu Matsuura, Taichi Murakami, Kojiro Nagai, Hideharu Abe, Yasuhiko Nishioka and Toshio Doi :
IgA Nephropathy after Nivolumab Therapy for Postoperative Recurrence of Lung Squamous Cell Carcinoma.,
Internal Medicine, Vol.57, No.9, 1259-1263, 2018.

(要約): Immune checkpoint inhibitors (ICIs) are becoming a common and important cancer therapy. ICIs are associated with a unique category of side effects, termed immune-related adverse events (irAEs). We herein report the case of a 72-year-old man with postoperative recurrence of lung squamous cell carcinoma who was treated with nivolumab and who developed proteinuria and a worsening kidney function. A kidney biopsy revealed IgA nephropathy. After drug withdrawal, the proteinuria improved and the deterioration of the patient's renal function was halted. Although renal irAEs are considered to be rare and glomerulonephritis is not typical presentation, physicians need to pay more attention to renal irAEs and glomerular injury.
(キーワード): Aged / Antibodies, Monoclonal / Antineoplastic Agents / Carcinoma, Squamous Cell / Glomerulonephritis, IGA / Humans / Lung Neoplasms / 男性 (male) / Neoplasm Recurrence, Local / Nivolumab / Proteinuria
(徳島大学機関リポジトリ): ● Metadata: 114399
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.9814-17
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29279511; ● Summary page in Scopus @ Elsevier: 2-s2.0-85046287943

(徳島大学機関リポジトリ: 114399, DOI: 10.2169/internalmedicine.9814-17, PubMed: 29279511, Elsevier: Scopus) Kojiro Nagai, Hiroyuki Ono, Motokazu Matsuura, Michael Hann, Sayo Ueda, Sakiya Yoshimoto, Masanori Tamaki, Taichi Murakami, Hideharu Abe, Hisashi Ishikura and Toshio Doi :
Progressive renal insufficiency related to ALK inhibitor, alectinib.,
Oxford Medical Case Reports, Vol.2018, No.4, 2018.

(要約): Alectinib is a second generation anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitor and is generally effective and tolerated in patients who have demonstrated disease progression or adverse effects while on the first generation inhibitor, crizotinib. ALK inhibitors can cause a reversible chronic increase of serum creatinine concentration; however, they rarely induce progressive renal insufficiency. We herein report a case of a 68-year-old woman diagnosed with ALK-positive advanced non-small cell lung cancer and who received ALK inhibitors. Due to dysgeusia and transaminitis, her medication was switched from crizotinib to alectinib. Rapid progressive glomerulonephritis developed 1 year after the initiation of alectinib treatment. A renal biopsy revealed unique kidney lesions in both tubules and glomeruli. Glucocorticoid therapy partially reversed kidney impairment. However, re-administration of alectinib caused kidney dysfunction, which was improved by the cessation of alectinib. Our case suggests that much attention should be paid to kidney function when using ALK inhibitors.
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/omcr/omy009
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29713488; ● Search Scopus @ Elsevier (PMID): 29713488; ● Search Scopus @ Elsevier (DOI): 10.1093/omcr/omy009

(DOI: 10.1093/omcr/omy009, PubMed: 29713488) Fumi Kishi, Kojiro Nagai, Norimichi Takamatsu, Tatsuya Tominaga, Masanori Tamaki, E. Shibata, Taichi Murakami, Seiji Kishi, Hideharu Abe, Y Koezuka, N Minagawa, G Ichien and Toshio Doi :
Urinary type IV collagen excretion is involved in the decline in estimated glomerular filtration rate in the Japanese general population without diabetes: A 5-year observational study.,
PLoS ONE, Vol.13, No.4, e0195523, 2018.

(要約): Urinary type IV collagen (U-Col4) and albumin excretion is evaluated to monitor the development of diabetic kidney disease. However, U-Col4 excretion in the general population without diabetes has not yet been fully elucidated. In this study, 1067 participants without diabetes and with urinary albumin-creatinine ratio <300 mg/gCr (normo- or microalbuminuria) who underwent an annual health examination in 2004 were enrolled and observed for 5 years. They were divided according to the amount of U-Col4 or urinary albumin excreted. The decline in estimated glomerular filtration rate (eGFR) was calculated. In participants with eGFR ≥80 mL/min, abnormal U-Col4 excretion was indicated as a significant independent risk factor for 10% eGFR change per year, which is one of the prognostic factors for the development of end-stage kidney disease. Moreover, in contrast to urinary albumin excretion, U-Col4 excretion was not related to age or kidney function, suggesting that some individuals with abnormal U-Col4 excretion can have an independent hidden risk for the development of kidney dysfunction. In conclusion, it is important to measure U-Col4 excretion in the general population without diabetes to determine changes in renal features in every individual and help detect future complications such as diabetic kidney disease. If U-Col4 excretion is abnormal, kidney manifestation should be carefully followed up, even if the kidney function and urinalysis findings are normal.
(キーワード): Adult / Aged / Aged, 80 and over / Albuminuria / Asian Continental Ancestry Group / Collagen Type IV / Diabetic Nephropathies / Disease Progression / Female / Glomerular Filtration Rate / Humans / Japan / Kaplan-Meier Estimate / Male / Middle Aged / Prognosis / Renal Insufficiency / Risk Factors / Young Adult
(徳島大学機関リポジトリ): ● Metadata: 112361
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0195523
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29624611; ● Search Scopus @ Elsevier (PMID): 29624611; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0195523

(徳島大学機関リポジトリ: 112361, DOI: 10.1371/journal.pone.0195523, PubMed: 29624611) Toshio Doi, Hideharu Abe, Seiji Kishi, Taichi Murakami, Kojiro Nagai and Tatsuya Tominaga :
Urinary IgG4 and Smad1 are Specific Biomarkers for Renal Structural and Functional Changes in Early Stages of Diabetic Nephropathy.,
Diabetes, Vol.67, No.5, 986-993, 2018.

(要約): Diabetic nephropathy (DN) is the major cause of end-stage kidney disease, but early biomarkers of DN risk are limited. Herein we examine urinary IgG4 and Smad1 as additional early DN biomarkers. We recruited 815 patients with type 2 diabetes; 554 patients fulfilled the criteria of an estimated glomerular filtration rate (eGFR) >60 mL/min and no macroalbuminuria at baseline, with follow-up for 5 years. Patients without macroalbuminuria were also recruited for renal biopsies. Urinary IgG4 and Smad1 were determined by enzyme-linked immunoassays using specific antibodies. The specificity, sensitivity, and reproducibility were confirmed for each assay. Increased urinary IgG4 was significantly associated with lower eGFR. The level of urinary IgG4 also significantly correlated with surface density of peripheral glomerular basement membrane (Sv PGBM/Glom), whereas Smad1 was associated with the degree of mesangial expansion-both classic pathological findings in DN. Baseline eGFR did not differ between any groups; however, increases in both urinary IgG4 and Smad1 levels at baseline significantly predicted later development of eGFR decline in patients without macroalbuminuria. These data suggest that urinary IgG4 and Smad1 at relatively early stages of DN reflect underlying DN lesions and are relevant to later clinical outcomes.
(キーワード): Adult / Biomarkers / Diabetes Mellitus, Type 2 / Diabetic Nephropathies / Early Diagnosis / Enzyme-Linked Immunosorbent Assay / Female / Glomerular Basement Membrane / Glomerular Filtration Rate / Humans / Immunoglobulin G / Kidney / Male / Mesangial Cells / Microscopy, Electron / Middle Aged / Reproducibility of Results / Sensitivity and Specificity / Smad1 Protein
(出版サイトへのリンク): ● Publication site (DOI): 10.2337/db17-1043
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29490904; ● Search Scopus @ Elsevier (PMID): 29490904; ● Search Scopus @ Elsevier (DOI): 10.2337/db17-1043

(DOI: 10.2337/db17-1043, PubMed: 29490904) Hideharu Abe and Tatsuya Tominaga :
New insights into the molecular pathology and the development of predictive biomarkers in diabetic mephropathy.,
Trends in Cell & Molecular Biology, Vol.13, No.4, 19-26, 2018. Hiroyuki Ono, Kojiro Nagai, Eriko Shibata, Motokazu Matsuura, Seiji Kishi, Taizo Inagaki, Masanori Minato, Sakiya Yoshimoto, Sayo Ueda, Fumiaki Obata, Kenji Nishimura, Masanori Tamaki, Fumi Kishi, Taichi Murakami, Hideharu Abe, Yukiko Kinoshita, Maki Urushihara, Shoji Kagami and Toshio Doi :
Re-recognition of Age-dependent Reference Range for the Serum Creatinine Level in Teenagers - A Case of Slowly Progressive Tubulointerstitial Nephritis which Occurred in an Adolescent.,
Internal Medicine, Vol.56, No.16, 2187-2193, 2017.

(要約): For the first time, a 15-year-old boy was found to have a slight degree of proteinuria and microscopic hematuria during annual school urinalysis screening. His kidney function had already severely deteriorated. A kidney biopsy revealed tubulointerstitial nephritis (TIN) with diffuse inflammatory cell infiltration. His medical records showed his serum creatinine level to be 0.98 mg/dL two years ago, which was abnormally high considering his age. Although the etiology of slowly progressive TIN was unclear, glucocorticoid and immunosuppressant therapy improved his kidney function. This case report suggests that all doctors should recognize the reference range for the serum creatinine level in teenagers.
(徳島大学機関リポジトリ): ● Metadata: 114406
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.8599-16
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28781321; ● Search Scopus @ Elsevier (PMID): 28781321; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.8599-16

(徳島大学機関リポジトリ: 114406, DOI: 10.2169/internalmedicine.8599-16, PubMed: 28781321) Hiroyuki Ono, Taichi Murakami, Akira Mima, Eriko Shibata, Masanori Tamaki, Sakiya Yoshimoto, Sayo Ueda, Fumi Kishi, Seiji Kishi, Takashi Kawanaka, Motokazu Matsuura, Kojiro Nagai, Hideharu Abe, Masashi Harada and Toshio Doi :
Successful treatment of highly advanced immunoglobulin G4-related kidney disease presenting renal mass-like regions with end-stage kidney failure: a case study.,
BMC Nephrology, Vol.18, No.1, 261, 2017.

(要約): A 59-year-old Japanese man was referred to our hospital because of uremia with a creatinine level of 12.36 mg/dL. Urinalysis revealed mild proteinuria and hyperβ2microglobulinuria, and blood tests showed hyperglobulinemia with an IgG level of 3243 mg/dL and an IgG4 level of 621 mg/dL. Non-contrast computed tomography revealed renal mass-like regions. Based on the findings, immunoglobulin G4-related kidney disease was suspected, however, further radiological examination showed unexpected results. Ga-67 scintigraphy showed no kidney uptake. T2-weighted magnetic resonance imaging revealed high-intensity signals which corresponded to mass-like regions and multiple patchy low-intensity signals in kidney cortex. Finally, the patient was diagnosed with immunoglobulin G4-related kidney disease by renal pathology of severe immunoglobulin G4-positive plasma cell-rich tubulointerstitial nephritis and characteristic fibrosis. He received 50 mg oral prednisolone, which was tapered with a subsequent decrease of serum creatinine and IgG4 levels. One year after initiation of treatment, he achieved normalization of serum IgG4 level and proteinuria, and remained off dialysis with a creatinine level of 3.50 mg/dL. After treatment with steroids, repeat imaging suggested bilateral severe focal atrophy. However, mass-like regions did not show atrophic change although renal atrophy was evident in patchy low-intensity lesions on T2-weighted magnetic resonance imaging. These findings suggest that multiple patchy low-intensity signals and high-intensity mass-like regions were mildly atrophic lesions of immunoglobulin G4-related kidney disease due to severe fibrosis and normal parts of kidney, respectively.
(徳島大学機関リポジトリ): ● Metadata: 114372
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/s12882-017-0676-5
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28774276; ● Search Scopus @ Elsevier (PMID): 28774276; ● Search Scopus @ Elsevier (DOI): 10.1186/s12882-017-0676-5

(徳島大学機関リポジトリ: 114372, DOI: 10.1186/s12882-017-0676-5, PubMed: 28774276) Kojiro Nagai, Tatsuya Tominaga, Sayo Ueda, Eriko Shibata, Masanori Tamaki, Motokazu Matsuura, Seiji Kishi, Taichi Murakami, Tatsumi Moriya, Hideharu Abe and Toshio Doi :
Mesangial Cell Mammalian Target of Rapamycin Complex 1 Activation Results in Mesangial Expansion.,
Journal of the American Society of Nephrology, Vol.28, No.10, 2879-2885, 2017.

(要約): Human glomerular diseases can be caused by several different diseases, many of which include mesangial expansion and/or proliferation followed by glomerulosclerosis. However, molecular mechanisms underlying the pathologic mesangial changes remain poorly understood. Here, we investigated the role of the mammalian target of rapamycin complex 1 (mTORC1)-S6 kinase pathway in mesangial expansion and/or proliferation by ablating an upstream negative regulator, tuberous sclerosis complex 1 (TSC1), using tamoxifen-induced Foxd1-Cre mice [Foxd1ER(+) TSC1 mice]. Foxd1ER(+) TSC1 mice showed mesangial expansion with increased production of collagen IV, collagen I, and -smooth muscle actin in glomeruli, but did not exhibit significant mesangial proliferation or albuminuria. Furthermore, rapamycin treatment of Foxd1ER(+) TSC1 mice suppressed mesangial expansion. Among biopsy specimens from patients with glomerular diseases, analysis of phosphorylated ribosomal protein S6 revealed mesangial cell mTORC1 activation in IgA nephropathy and in lupus mesangial proliferative nephritis but not in the early phase of diabetic nephropathy. In summary, mesangial cell mTORC1 activation can cause mesangial expansion and has clinical relevance for human glomerular diseases. This report also confirms that the tamoxifen-induced mesangium-specific Cre-loxP system is useful for studies designed to clarify the role of the mesangium in glomerular diseases in adults.
(出版サイトへのリンク): ● Publication site (DOI): 10.1681/ASN.2016111196
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28701517; ● Summary page in Scopus @ Elsevier: 2-s2.0-85030471083

(DOI: 10.1681/ASN.2016111196, PubMed: 28701517, Elsevier: Scopus) Hiroyuki Ono, Seiji Kishi, Taizo Inagaki, Masako Mizusawa, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi :
Shunt nephritis and pyogenic spondylitis with a positive PR3-ANCA associated with chronically infected ventriculo-atrial shunt,
Kidney International Reports, Vol.2, No.4, 774-778, 2017.

(徳島大学機関リポジトリ): ● Metadata: 114987
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ekir.2017.02.013
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1016/j.ekir.2017.02.013

(徳島大学機関リポジトリ: 114987, DOI: 10.1016/j.ekir.2017.02.013) Hideharu Abe, Akiko Sakurai and Toshio Doi :
Probucol modulates Nrf2 function and ameliorates diabetic nephropathy in db/db mice.,
Medical Research Archives, Vol.10, No.4, 1-16, 2017.

(出版サイトへのリンク): ● Publication site (DOI): 10.18103/mra.v4i8.935
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.18103/mra.v4i8.935

(DOI: 10.18103/mra.v4i8.935) Motokazu Matsuura, Hideharu Abe, Tatsuya Tominaga, Akiko Sakurai, Taichi Murakami, Seiji Kishi, Yoshimi Bando, Jun Minakuchi, Kojiro Nagai and Toshio Doi :
A Novel Method of DAPI Staining for Differential Diagnosis of Renal Amyloidosis.,
The Journal of Medical Investigation : JMI, Vol.64, No.3.4, 217-221, 2017.

(要約): Amyloidosis is often overlooked because its clinical manifestations can mimic those of more-common diseases. It is important to get a precise diagnosis as early as possible for the prevention of further organ damages. Amyloidosis is a disorder caused by deposition of insoluble abnormal amyloid. The kidney is a frequent site of amyloid deposition. The amyloid fibrils have a characteristic appearance and generate birefringence under polarized light when stained with the Congo red dye. Classification of amyloidosis is based on the precursor protein that forms the amyloid fibrils and the distribution of amyloid deposits as either systemic or localized. Involvement of amyloid fibrils in kidneys mainly occurs as amyloid light-chain (AL) or amyloid A (AA) amyloidosis. The potassium permanganate method with Congo red staining was once used widely to discriminate AL and AA amyloidoses, but this method has a problem of false positive results. We found that extracellular and cytoplasmic glomerular 4', 6-diamidino-2-phenylindole (DAPI)-positive areas were clearly consistent with amyloid deposition in AL amyloidosis. In contrast, the overlapping staining was not seen in AA amyloidosis. Therefore, we propose that DAPI staining readily distinguishes AL renal amyloidosis from AA renal amyloidosis as a simple and reproducible histochemical method. J. Med. Invest. 64: 217-221, August, 2017.
(キーワード): Amyloidosis / Kidney Diseases / Serum Amyloid A Protein / Staining and Labeling
(徳島大学機関リポジトリ): ● Metadata: 111119
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.64.217
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28954985; ● Search Scopus @ Elsevier (PMID): 28954985; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.217

(徳島大学機関リポジトリ: 111119, DOI: 10.2152/jmi.64.217, PubMed: 28954985) Sakiya Yoshimoto, Kojiro Nagai, Eriko Shibata, Sayo Ueda, Hiroyuki Ono, Masanori Tamaki, Kenji Nishimura, Fumiaki Obata, Taizo Inagaki, Masanori Minato, Fumi Kishi, Motokazu Matsuura, Naoko Matsui, Itsuro Endo, Michael Hann, Seiji Kishi, Taichi Murakami, Hideharu Abe and Toshio Doi :
Influential factors on serum albumin concentration in hospitalized chronic kidney disease patients.,
The Journal of Medical Investigation : JMI, Vol.64, No.1.2, 146-152, 2017.

(要約): SAC was affected by not only proteinuria, but also postural change, physical activity, and food in CKD patients. SAC should be analyzed by standardizing a patient's condition during phlebotomy. J. Med. Invest. 64: 146-152, February, 2017.
(徳島大学機関リポジトリ): ● Metadata: 111103
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.64.146
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28373613; ● Search Scopus @ Elsevier (PMID): 28373613; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.146

(徳島大学機関リポジトリ: 111103, DOI: 10.2152/jmi.64.146, PubMed: 28373613) Fumiaki Obata, Taichi Murakami, Junko Miyagi, Sayo Ueda, Taizo Inagaki, Masanori Minato, Hiroyuki Ono, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Sakiya Yoshimoto, Fumi Kishi, Seiji Kishi, Motokazu Matsuura, Kojiro Nagai, Hideharu Abe and Toshio Doi :
A case of rapid amelioration of hepatitis C virus-associated cryoglobulinemic membranoproliferative glomerulonephritis treated by interferon-free directly acting antivirals for HCV in the absence of immunosuppressant.,
CEN Case Reports, Vol.6, No.1, 55-60, 2016.

(要約): Mixed cryoglobulinemic syndrome, which is a systemic vasculitis characterized by the immune complex deposition in small- and medium-sized arteries and most often due to chronic hepatitis C virus (HCV) infection, sometimes clinically manifests as refractory glomerulonephritis or nephritic syndrome. Patients with mixed cryoglobulinemic nephropathy who have a rapidly progressive glomerulonephritis should receive immunosuppressive therapy. After disease stabilization, patients should receive concurrent therapy for the underlying HCV infection. The standard therapy of a chronic HCV infection is IFN monotherapy or IFN combined with ribavirin; however, after the introduction of direct-acting antivirals (DAAs), the standard therapy for patients with HCV genotype 1 has dramatically changed. We report a case of HCV-associated cryoglobulinemic membranoproliferative glomerulonephritis (MPGN) successfully treated by daclatasvir and asunaprevir, which are IFN-free DAAs for HCV, in combination with angiotensin II receptor blocker without immunosuppressive therapy. The patient developed severe nephrotic syndrome with progressive kidney dysfunction. Blood examination revealed a high copy number of HCV-RNA (6.4 log IU/mL, type 1), cryoglobulinemia, paraproteinemia of IgM-, and hypocomplementemia. Histological analysis showed MPGN type 1. These findings were compatible with those observed in HCV-associated cryoglobulinemic MPGN. This case offers original evidence for the application of newer generation of IFN-free DAAs in the treatment of HCV-associated cryoglobulinemic nephropathy.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s13730-016-0244-z
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28509128; ● Search Scopus @ Elsevier (PMID): 28509128; ● Search Scopus @ Elsevier (DOI): 10.1007/s13730-016-0244-z

(DOI: 10.1007/s13730-016-0244-z, PubMed: 28509128) Takahiro Hirano, Taichi Murakami, Hiroyuki Ono, Akiko Sakurai, Tatsuya Tominaga, Toshikazu Takahashi, Kojiro Nagai, Toshio Doi and Hideharu Abe :
A Novel Interaction between FLICE-Associated Huge Protein (FLASH) and E2A Regulates Cell Proliferation and Cellular Senescence via Tumor Necrosis Factor (TNF)-Alpha-p21WAF1/CIP1 Axis.,
PLoS ONE, Vol.10, No.7, e0133205, 2015.

(要約): Dysregulation of the cell proliferation has been implicated in the pathophysiology of a number of diseases. Cellular senescence limits proliferation of cancer cells, preventing tumorigenesis and restricting tissue damage. However, the role of cellular senescence in proliferative nephritis has not been determined. The proliferative peak in experimental rat nephritis coincided with a peak in E2A expression in the glomeruli. Meanwhile, E12 (an E2A-encoded transcription factor) did not promote proliferation of Mesangial cells (MCs) by itself. We identified caspase-8-binding protein FLICE-associated huge protein (FLASH) as a novel E2A-binding partner by using a yeast two-hybrid screening. Knockdown of FLASH suppressed proliferation of MCs. This inhibitory effect was partially reversed by the knockdown of E2A. In addition, the knockdown of FLASH induced cyclin-dependent kinase inhibitor p21WAF1/CIP1 (p21) expression, but did not affect p53 expression. Furthermore, overexpression of E12 and E47 induced p21, but not p53 in MCs, in the absence of FLASH. We also demonstrated that E2A and p21 expression at the peak of proliferation was followed by significant induction of FLASH in mesangial areas in rat proliferative glomerulonephritis. Moreover, we revealed that FLASH negatively regulates cellular senescence via the interaction with E12. We also demonstrated that FLASH is involved in the TNF--induced p21 expressions. These results suggest that the functional interaction of E2A and FLASH play an important role in cell proliferation and cellular senescence via regulation of p21 expression in experimental glomerulonephritis.
(徳島大学機関リポジトリ): ● Metadata: 114923
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0133205
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26208142; ● Summary page in Scopus @ Elsevier: 2-s2.0-84941908247

(徳島大学機関リポジトリ: 114923, DOI: 10.1371/journal.pone.0133205, PubMed: 26208142, Elsevier: Scopus) Takeshi Matsubara, Makoto Araki, Hideharu Abe, Otoya Ueda, Kou-Ichi Jishage, Akira Mima, Chisato Goto, Tatsuya Tominaga, Masahiko Kinosaki, Seiji Kishi, Kojiro Nagai, Noriyuki Iehara, Naoshi Fukushima, Toru Kita, Hidenori Arai and Toshio Doi :
Bone Morphogenetic Protein 4 and Smad1 Mediate Extracellular Matrix Production in the Development of Diabetic Nephropathy.,
Diabetes, Vol.64, No.8, 2978-2990, 2015.

(要約): Diabetic nephropathy is the leading cause of end-stage renal disease. It is pathologically characterized by the accumulation of extracellular matrix in the mesangium, of which the main component is 1/2 type IV collagen (Col4a1/a2). Recently, we identified Smad1 as a direct regulator of Col4a1/a2 under diabetic conditions in vitro. Here, we demonstrate that Smad1 plays a key role in diabetic nephropathy through bone morphogenetic protein 4 (BMP4) in vivo. Smad1-overexpressing mice (Smad1-Tg) were established, and diabetes was induced by streptozotocin. Nondiabetic Smad1-Tg did not exhibit histological changes in the kidney; however, the induction of diabetes resulted in an 1.5-fold greater mesangial expansion, consistent with an increase in glomerular phosphorylated Smad1. To address regulatory factors of Smad1, we determined that BMP4 and its receptor are increased in diabetic glomeruli and that diabetic Smad1-Tg and wild-type mice treated with a BMP4-neutralizing antibody exhibit decreased Smad1 phosphorylation and 40% less mesangial expansion than those treated with control IgG. Furthermore, heterozygous Smad1 knockout mice exhibit attenuated mesangial expansion in the diabetic condition. The data indicate that BMP4/Smad1 signaling is a critical cascade for the progression of mesangial expansion and that blocking this signal could be a novel therapeutic strategy for diabetic nephropathy.
(出版サイトへのリンク): ● Publication site (DOI): 10.2337/db14-0893
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25995358; ● Summary page in Scopus @ Elsevier: 2-s2.0-84943360079

(DOI: 10.2337/db14-0893, PubMed: 25995358, Elsevier: Scopus) Eriko Shibata, Kojiro Nagai, Risa Takeuchi, Yasuhiro Noda, Tomomi Makino, Yusuke Chikata, Michael Hann, Sakiya Yoshimoto, Hiroyuki Ono, Sayo Ueda, Masanori Tamaki, Taichi Murakami, Motokazu Matsuura, Hideharu Abe and Toshio Doi :
Re-evaluation of Pre-pump Arterial Pressure to Avoid Inadequate Dialysis and Hemolysis: Importance of Prepump Arterial Pressure Monitoring in Hemodialysis Patients.,
Artificial Organs, Vol.39, No.7, 627-634, 2015.

(要約): Prepump arterial pressure (PreAP) is monitored to avoid generating excessive negative pressure. The National Kidney Foundation K/DOQI clinical practice guidelines for vascular access recommend that PreAP should not fall below -250 mm Hg because excessive negative PreAP can lead to a decrease in the delivery of blood flow, inadequate dialysis, and hemolysis. Nonetheless, these recommendations are consistently disregarded in clinical practice and pressure sensors are often removed from the dialysis circuit. Thus far, delivered blood flow has been reported to decrease at values more negative than -150 mm Hg of PreAP. These values have been analyzed by an ultrasonic flowmeter and not directly measured. Furthermore, no known group has evaluated whether PreAP-induced hemolysis occurs at a particular threshold. Therefore, the aim of this study was to clarify the importance of PreAP in the prediction of inadequate dialysis and hemolysis. By using different diameter needles, human blood samples from healthy volunteers were circulated in a closed dialysis circuit. The relationship between PreAP and delivered blood flow or PreAP and hemolysis was investigated. We also investigated the optimal value for PreAP using several empirical monitoring methods, such as a pressure pillow. Our investigation indicated that PreAP is a critical factor in the determination of delivered blood flow and hemolysis, both of which occured at pressure values more negative than -150 mm Hg. With the exception of direct pressure monitoring, commonly used monitoring methods for PreAP were determined to be ineffective. We propose that the use of a vacuum monitor would permit regular measurement of PreAP.
(徳島大学機関リポジトリ): ● Metadata: 110961
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/aor.12448
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25940509; ● Summary page in Scopus @ Elsevier: 2-s2.0-84934324257

(徳島大学機関リポジトリ: 110961, DOI: 10.1111/aor.12448, PubMed: 25940509, Elsevier: Scopus) Kengo Furuichi, Miho Shimizu, Tadashi Toyama, Daisuke Koya, Yoshitaka Koshino, Hideharu Abe, Kiyoshi Mori, Hiroaki Satoh, Masahito Imanishi, Masayuki Iwano, Hiroyuki Yamauchi, Eiji Kusano, Shouichi Fujimoto, Yoshiki Suzuki, Seiya Okuda, Kiyoki Kitagawa, Yasunori Iwata, Shuichi Kaneko, Shinichi Nishi, Hitoshi Yokoyama, Yoshihiko Ueda, Masakazu Haneda, Hirofumi Makino and Takashi Wada :
Japan Diabetic Nephropathy Cohort Study: study design, methods, and implementation.,
Clinical and Experimental Nephrology, Vol.17, No.6, 819-826, 2013.

(要約): We analyzed the data of 321 participants (106 female, 215 male; average age 65 years) in the JDNCS. Systolic and diastolic blood pressure was 130.1 and 72.3 mmHg, respectively. Median estimated glomerular filtration rate (eGFR) was 33.3 ml/min/1.73 m(2). Proteinuria was 1.8 g/gCr, and serum levels of albumin were 3.6 g/dl. The majority of the JDNCS patients presented with preserved eGFR and low albuminuria or low eGFR and advanced proteinuria. In the JRBR and JKDR registries, 484 and 125 participants, respectively, were enrolled as having diabetes mellitus. In comparison with the JRBR and JKDR registries, the JDNCS was characterized by diabetic patients presenting with low proteinuria with moderately preserved eGFR.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10157-013-0778-8
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23446518; ● Summary page in Scopus @ Elsevier: 2-s2.0-84891486926

(DOI: 10.1007/s10157-013-0778-8, PubMed: 23446518, Elsevier: Scopus) Kazuhiro Yoshikawa, Hideharu Abe, Tatsuya Tominaga, Masayuki Nakamura, Seiji Kishi, Motokazu Matsuura, Kojiro Nagai, Kenji Tsuchida, Jun Minakuchi and Toshio Doi :
Polymorphism in the human matrix Gla protein gene is associated with the progression of vascular calcification in maintenance hemodialysis patients,
Clinical and Experimental Nephrology, Vol.17, No.6, 882-889, 2013.

(要約): Matrix Gla protein (MGP) is one of the important proteins inhibiting vascular calcification (VC). Single nucleotide polymorphisms (SNPs) located in the promoter and coding regions of the MGP gene affect the transcriptional activity. In this study, we investigated the relationship between the SNPs and progression of VC in patients undergoing maintenance hemodialysis (MHD). This was a retrospective, longitudinal cohort study of 134 MHD patients whose VC could be followed by multi-detector computed tomography (MDCT) examinations. MGP-SNPs (T-138C, rs1800802 and G-7A, rs1800801) were determined. The progression speed of VC was examined by plotting the abdominal aortic calcium volume scores. The progression speed of VC of patients with the CC genotype of T-138C was significantly slower than that of patients with the CT or TT genotype. Multiple regression analysis showed that CT/TT genotype, greater age at the beginning of MHD, male sex, high levels of calcium × phosphate, low levels of high-density lipoprotein cholesterol, high levels of low-density lipoprotein cholesterol, low levels of ferritin and non-use of angiotensin II receptor blockers were significantly associated with progression of VC. The MGP-138CC genotype may be associated with slower progression of VC in MHD patients. The genotype of the MGP gene will be a genomic biomarker that is predictive of VC progression.
(徳島大学機関リポジトリ): ● Metadata: 105885
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10157-013-0785-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23504408; ● Summary page in Scopus @ Elsevier: 2-s2.0-84891483720

(徳島大学機関リポジトリ: 105885, DOI: 10.1007/s10157-013-0785-9, PubMed: 23504408, Elsevier: Scopus) Kojiro Nagai, Masashi Miyoshi, Takei Kake, Naoshi Fukushima, Motokazu Matsuura, Eriko Shibata, Satoshi Yamada, Kazuhiro Yoshikawa, Hiro-omi Kanayama, Tomoya Fukawa, Kunihisa Yamaguchi, Hirofumi Izaki, Akira Mima, Naoko Abe, Toshikazu Araoka, Taichi Murakami, Fumi Kishi, Seiji Kishi, Tatsuya Tominaga, Tatsumi Moriya, Hideharu Abe and Toshio Doi :
Dual Involvement of Growth Arrest-specific Gene 6 in the Early Phase of Human IgA Nephropathy,
PLoS ONE, Vol.8, No.6, e66759, 2013.

(要約): Gas6 is a growth factor that causes proliferation of mesangial cells in the development of glomerulonephritis. Gas6 can bind to three kinds of receptors; Axl, Dtk, and Mer. However, their expression and functions are not entirely clear in the different glomerular cell types. Meanwhile, representative cell cycle regulatory protein p27 has been reported to be expressed in podocytes in normal glomeruli with decreased expression in proliferating glomeruli, which inversely correlated with mesangial proliferation in human IgA nephropathy (IgAN). The aim of this study is to clarify Gas6 involvement in the progression of IgAN. Expression of Gas6/Axl/Dtk was examined in 31 biopsy proven IgAN cases. We compared the expression levels with histological severity or clinical data. Moreover, we investigated the expression of Gas6 and its receptors in cultured podocytes. In 28 of 31 cases, Gas6 was upregulated mainly in podocytes. In the other 3 cases, Gas6 expression was induced in endothelial and mesangial cells, which was similar to animal nephritis models. Among 28 podocyte type cases, the expression level of Gas6 correlated with the mesangial hypercellularity score of IgAN Oxford classification and urine protein excretion. It also inversely correlated with p27 expression in glomeruli. As for the receptors, Axl was mainly expressed in endothelial and mesangial cells, while Dtk was expressed in podocytes. In vitro, Dtk was expressed in cultured murine podocytes, and the expression of p27 was decreased by Gas6 stimulation. Gas6 was uniquely upregulated in either endothelial/mesangial cells or podocytes in IgAN. The expression pattern can be used as a marker to classify IgAN. Gas6 has a possibility to be involved in not only mesangial proliferation via Axl, but also podocyte injury via Dtk in IgAN.
(キーワード): Cells, Cultured / Endothelial Cells / Glomerulonephritis, IGA / Humans / Immunohistochemistry / Intercellular Signaling Peptides and Proteins / Mesangial Cells / Podocytes
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0066759
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23826128; ● Summary page in Scopus @ Elsevier: 2-s2.0-84879474790

(DOI: 10.1371/journal.pone.0066759, PubMed: 23826128, Elsevier: Scopus) Seiji Kishi, Satoshi Yamada, Fumi Kishi, Eriko Shibata, Motokazu Matsuura, Kojiro Nagai, Akira Mima, Hideharu Abe and Toshio Doi :
Acute Glomerulonephritis in an Immunocompetent Elderly Woman after Contact with a Child who Had Been Diagnosed as Erythema Infectiosum.,
Internal Medicine, Vol.51, No.16, 2197-2201, 2012.

(要約): The prevalence of postinfectious glomerulonephritis has decreased in most developed countries. We report the case of a previously healthy, immunocompetent 65-year-old woman who developed acute glomerulonephritis associated with human parvovirus B19 infection. She was referred by her primary care physician for suspected congestive heart failure but she had an elevated creatinine level and an abnormal urinalysis. Renal biopsy showed diffuse endocapillary proliferative glomerulonephritis. After biopsy, we learned that she had been in frequent contact with her grandson who had been diagnosed with erythema infectiosum. Her human parvovirus B19 serum IgM titer was elevated at 3.50, indicating current infection.
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.51.7919
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22892503; ● Search Scopus @ Elsevier (PMID): 22892503; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.51.7919

(DOI: 10.2169/internalmedicine.51.7919, PubMed: 22892503) Kazuo Torikoshi, Hideharu Abe, Takeshi Matsubara, Takahiro Hirano, Takayuki Ohshima, Taichi Murakami, Makoto Araki, Akira Mima, Noriyuki Iehara, Atsushi Fukatsu, Toru Kita, Hidenori Arai and Toshio Doi :
Protein Inhibitor of Activated STAT, PIASy Regulates α-Smooth Muscle Actin Expression by Interacting with E12 in Mesangial Cells.,
PLoS ONE, Vol.7, No.7, e41186, 2012.

(要約): Phenotypic transformation of mesangial cells (MCs) is implicated in the development of glomerular disease; however, the mechanisms underlying their altered genetic program is still unclear. α-smooth muscle actin (α-SMA) is known to be a crucial marker for phenotypic transformation of MCs. Recently, E-boxes and the class I basic helix-loop-helix proteins, such as E12 have been shown to regulateα-SMA expression. Therefore, we tried to identify a novel E12 binding protein in MCs and to examine its role in glomerulonephritis. We found that PIASy, one of the protein inhibitors of activated STAT family protein, interacted with E12 by yeast two-hybrid screens and coimmunopreciptation assays. Overexpression of E12 significantly enhanced theα-SMA promoter activity, and the increase was blocked by co-transfection of PIASy, but not by a PIASy RING mutant. In vivo sumoylation assays revealed that PIASy was a SUMO E3 ligase for E12. Furthermore, transforming growth factor-β (TGF-β) treatment induced expression of both PIASy and E12, consistent with α-SMA expression. Moreover, reduced expression of PIASy protein by siRNA specific for PIASy resulted in increased TGF-β-mediated α-SMA expression. In vivo, PIASy and E12 were dramatically upregulated along with α-SMA and TGF-β in the proliferative phase of Thy1 glomerulonephritis. Furthermore, an association between PIASy and E12 proteins was observed at day 6 by IP-western blotting, but not at day 0. These results suggest that TGF-β up-regulates PIASy expression in MCs to down-regulateα-SMA gene transcription by the interaction with E12.
(キーワード): Actins / Animals / Blotting, Western / COS Cells / Cell Line / Cell Proliferation / Humans / 免疫組織化学 (immunohistochemistry) / Immunoprecipitation / Male / Mesangial Cells / Protein Binding / Protein Inhibitors of Activated STAT / RNA Interference / Rats / Rats, Inbred WKY / Reverse Transcriptase Polymerase Chain Reaction / Transcription Factor 3 / Two-Hybrid System Techniques
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0041186
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22829926; ● CiNii @ 国立情報学研究所 (CRID): 1050564285690802944; ● Search Scopus @ Elsevier (PMID): 22829926; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0041186

(DOI: 10.1371/journal.pone.0041186, PubMed: 22829926, CiNii: 1050564285690802944) 柴田恵理子, 長井幸二郎, 松浦元一, 山田諭, 渡瀬謙仁, 岸史, 美馬晶, 岸誠司, 安部秀斉, 土井俊夫 :
中等度以上腎機能低下患者に対するフェブキソスタットの有効性と認容性の検討,
Therapeutic research, Vol.33, No.7, 1073-1080, 2012年. Hideharu Abe, Tatsuya Tominaga, Takeshi Matsubara, Naoko Abe, Seiji Kishi, Kojiro Nagai, Taichi Murakami, Toshikazu Araoka and Toshio Doi :
Scleraxis modulates bone morphogenetic protein 4 (BMP4)-Smad1 protein-smooth muscle -actin (SMA) signal transduction in diabetic nephropathy.,
The Journal of Biological Chemistry, Vol.287, No.24, 20430-20442, 2012.

(要約): Activation of mesangial cells (MCs), which is characterized by induction of smooth muscle -actin (SMA) expression, contributes to a key event in various renal diseases; however, the mechanisms controlling MC differentiation are still largely undefined. Activated Smad1 induced SMA in a dose-dependent manner in MCs. As a direct regulating molecule for SMA, we identified and characterized scleraxis (Scx) as a new phenotype modulator in advanced glycation end product (AGE)-exposed MCs. Scx physically associated with E12 and bound the E-box in the promoter of SMA and negatively regulated the AGE-induced SMA expression. Scx induced expression and secretion of bone morphogenetic protein 4 (BMP4), thereby controlling the Smad1 activation in AGE-treated MCs. In diabetic mice, Scx was concomitantly expressed with SMA in the glomeruli. Inhibitor of differentiation 1 (Id1) was further induced by extended treatment with AGE, thereby dislodging Scx from the SMA promoter. These data suggest that Scx and Id1 are involved in the BMP4-Smad1-SMA signal transduction pathway besides the TGF1-Smad1-SMA signaling pathway and modulate phenotypic changes in MCs in diabetic nephropathy.
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M111.275610
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22474292; ● Search Scopus @ Elsevier (PMID): 22474292; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M111.275610

(DOI: 10.1074/jbc.M111.275610, PubMed: 22474292) Seiji Kishi, Hideharu Abe, Haruhiko Akiyama, Tatsuya Tominaga, Taichi Murakami, Akira Mima, Kojiro Nagai, Fumi Kishi, Motokazu Matsuura, Takeshi Matsubara, Noriyuki Iehara, Otoya Ueda, Naoshi Fukushima, Kou-Ichi Jishage and Toshio Doi :
SOX9 protein induces a chondrogenic phenotype of mesangial cells and contributes to advanced diabetic nephropathy.,
The Journal of Biological Chemistry, Vol.286, No.37, 32162-32169, 2011.

(要約): Diabetic nephropathy (DN) is the most important chronic kidney disease. We previously reported that Smad1 transcriptionally regulates the expression of extracellular matrix in DN. Phenotypic change in mesangial cells (MCs) is a key pathologic event in the progression of DN. The aim of this study is to investigate a novel mechanism underlying chondrogenic phenotypic change in MCs that results in the development of DN. MCs showed chondrogenic potential in a micromass culture, and BMP4 induced the expression of chondrocyte markers (SRY-related HMG Box 9 (SOX9) and type II collagen (COL2)). Advanced glycation end products induced the expression of chondrocyte marker proteins downstream from the BMP4-Smad1 signaling pathway in MCs. In addition, hypoxia also induced the expression of BMP4, hypoxia-inducible factor-1 (HIF-1), and chondrocyte markers. Overexpression of SOX9 caused ectopic expression of proteoglycans and COL2 in MCs. Furthermore, forced expression of Smad1 induced chondrocyte markers as well. Dorsomorphin inhibited these inductions. Glomerular expressions of HIF-1, BMP4, and chondrocyte markers were observed in diabetic nephropathy mice. These positive stainings were observed in mesangial sclerotic lesions. SOX9 was partially colocalized with HIF-1 and BMP4 in diabetic glomeruli. BMP4 knock-in transgenic mice showed not only similar pathological lesions to DN, but also the induction of chondrocyte markers in the sclerotic lesions. Here we demonstrate that HIF-1 and BMP4 induce SOX9 expression and subsequent chondrogenic phenotype change in DN. The results suggested that the transdifferentiation of MCs into chondrocyte-like cells in chronic hypoxic stress may result in irreversible structural change in DN.
(キーワード): Animals / Antigens, Differentiation / Bone Morphogenetic Protein 4 / Cell Line / Cell Transdifferentiation / Chondrocytes / Collagen Type II / Diabetic Nephropathies / Gene Expression Regulation / Glomerular Mesangium / Glycosylation End Products, Advanced / Hypoxia-Inducible Factor 1, alpha Subunit / Mice / Mice, Transgenic / SOX9 Transcription Factor / Smad1 Protein
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M111.244541
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21795715; ● Search Scopus @ Elsevier (PMID): 21795715; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M111.244541

(DOI: 10.1074/jbc.M111.244541, PubMed: 21795715) 安部秀斉 :
糖尿病性腎症のターゲットと治療戦略,
臨床薬理, Vol.42, No.3, 179-186, 2011年.

(出版サイトへのリンク): ● Publication site (DOI): 10.3999/jscpt.42.189
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390282680344394112; ● Search Scopus @ Elsevier (DOI): 10.3999/jscpt.42.189

(DOI: 10.3999/jscpt.42.189, CiNii: 1390282680344394112) Akira Mima, Fumihiko Shiota, Takeshi Matsubara, Noriyuki Iehara, Taro Akagi, Hideharu Abe, Kojiro Nagai, Motokazu Matsuura, Taichi Murakami, Seiji Kishi, Toshikazu Araoka, Fumi Kishi, Naoki Kondo, Reiko Shigeta, Kazuhiro Yoshikawa, Toru Kita, Toshio Doi and Atsushi Fukatsu :
An autopsy case of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with intestinal bleeding in chronic renal failure.,
Renal Failure, Vol.33, No.6, 622-625, 2011.

(要約): A 50-year-old man who underwent hemodialysis (HD) at local outpatient HD center due to end-stage renal disease (ESRD) was transferred to our hospital because of pneumonia. He had severe emaciation and past history of congestive heart failure. Presenting symptoms almost consistently involved difficulty in hearing and recurrent attacks of migraine-like headaches. He was diagnosed with dilated cardiomyopathy, showing diastolic mechanical dyssynchrony by tissue Doppler echocardiography. On the day of death, he had hematemesis and hemorrhagic shock. Autopsy revealed perforation of duodenum, and genetic analysis using mitochondrial DNA from cardiac muscle and iliopsoas muscle revealed a 3243A > G mutation in the mitochondrial tRNA(Leu(UUR)) gene, which is related to mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Multiple organ failure due to the mutation of mitochondrial DNA with gastrointestinal bleeding is not a common.
(出版サイトへのリンク): ● Publication site (DOI): 10.3109/0886022X.2011.585730
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21631236; ● Search Scopus @ Elsevier (PMID): 21631236; ● Search Scopus @ Elsevier (DOI): 10.3109/0886022X.2011.585730

(DOI: 10.3109/0886022X.2011.585730, PubMed: 21631236) 安部秀斉 :
糖尿病性腎症の病因解析の進歩,
臨床病理, Vol.59, No.2, 179-186, 2011年.

(要約): Diabetic nephropathy (DN) is the leading cause of end-stage renal disease and a major contributor to morbidity and mortality of diabetic patients throughout the world. Albuminuria is one of the most characteristic functional changes in the early phase of DN. However, many recent studies have shown that there was no clear association between glomerulosclerosis and albuminuria in type 1 and 2 diabetes. DN is a progressive kidney disease caused by angiopathy of capillaries in the kidney glomeruli and is morphologically characterized by progressive expansion of mesangial matrix and thickening of the glomerular basement membrane. Type IV collagen (Col4) is a major component of the extracellular matrix (ECM) in the expanded mesangial matrix. Advanced glycation endproducts (AGEs) produced as the result of hyperglycemia are known to stimulate the production of ECM proteins in mesangial cells, resulting in glomerulosclerosis. Using a yeast one-hybrid screening, Smad1 was identified as a transcriptional regulator of Col4 in AGE-treated mesangial cells. Smad1 also regulated other ECM proteins, such as type I collagen and osteopontin, as well as alpha smooth muscle actin. Moreover, there was a very good correlation between urinary Smad1 levels and the development of mesangial expansion, whereas the correlation between albuminuria and mesangial expansion was not significant in experimental DN models. In addition, urinary Smad1 was revealed to be a good predictor for later onset of morphological changes and to be used to monitor the effect of ARB in DN. In conclusion, urinary Smad1 is expected to be a useful diagnostic biomarker for DN.
(キーワード): Albuminuria / Animals / Biological Markers / Collagen Type IV / Diabetic Nephropathies / Humans / Smad1 Protein
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21476304; ● CiNii @ 国立情報学研究所 (CRID): 1572543024889817856; ● Search Scopus @ Elsevier (PMID): 21476304

(PubMed: 21476304, CiNii: 1572543024889817856) Tatsuya Tominaga, Hideharu Abe, Otoya Ueda, Chisato Goto, Kunihiko Nakahara, Taichi Murakami, Takeshi Matsubara, Akira Mima, Kojiro Nagai, Toshikazu Araoka, Seiji Kishi, Naoshi Fukushima, Kou-ichi Jishage and Toshio Doi :
Activation of bone morphogenetic protein 4 signaling leads to glomerulosclerosis that mimics diabetic nephropathy.,
The Journal of Biological Chemistry, Vol.286, No.22, 20109-20116, 2011.

(要約): Diabetic nephropathy (DN) is the most common cause of chronic kidney disease. We have previously reported that Smad1 transcriptionally regulates the expression of extracellular matrix (ECM) proteins in DN. However, little is known about the regulatory mechanisms that induce and activate Smad1. Here, bone morphogenetic protein 4 (Bmp4) was found to up-regulate the expression of Smad1 in mesangial cells and subsequently to phosphorylate Smad1 downstream of the advanced glycation end product-receptor for advanced glycation end product signaling pathway. Moreover, Bmp4 utilized Alk3 and affected the activation of Smad1 and Col4 expressions in mesangial cells. In the diabetic mouse, Bmp4 was remarkably activated in the glomeruli, and the mesangial area was expanded. To elucidate the direct function of Bmp4 action in the kidneys, we generated transgenic mice inducible for the expression of Bmp4. Tamoxifen treatment dramatically induced the expression of Bmp4, especially in the glomeruli of the mice. Notably, in the nondiabetic condition, the mice exhibited not only an expansion of the mesangial area and thickening of the basement membrane but also remarkable albuminuria, which are consistent with the distinct glomerular injuries in DN. ECM protein overexpression and activation of Smad1 in the glomeruli were also observed in the mice. The mesangial expansion in the mice was significantly correlated with albuminuria. Furthermore, the heterozygous Bmp4 knock-out mice inhibited the glomerular injuries compared with wild type mice in diabetic conditions. Here, we show that BMP4 may act as an upstream regulatory molecule for the process of ECM accumulation in DN and thereby reveals a new aspect of the molecular mechanisms involved in DN.
(キーワード): Albuminuria / Animals / Bone Morphogenetic Protein 4 / Diabetic Nephropathies / 細胞外マトリックス (extracellular matrix) / Glomerulosclerosis, Focal Segmental / Glycosylation End Products, Advanced / Mesangial Cells / Mice / ノックアウトマウス (knockout mice) / Smad1 Protein / Up-Regulation
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M110.179382
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21471216; ● Search Scopus @ Elsevier (PMID): 21471216; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M110.179382

(DOI: 10.1074/jbc.M110.179382, PubMed: 21471216) Hideharu Abe, Takeshi Matsubara, Hidenori Arai and Toshio Doi :
Role of Smad1 in diabetic nephropathy: Molecular mechanisms and implications as a diagnostic marker.,
Histology and Histopathology, Vol.26, No.4, 531-541, 2011.

(要約): Diabetic nephropathy (DN) is the leading cause of chronic kidney failure. Moreover, DN is associated with elevated cardiovascular morbidity and mortality. DN is characterized by progressive expansion of the mesangial matrix and thickening of the glomerular basement membrane, resulting in the obliteration of glomerular capillaries. Advanced glycation endproducts (AGEs) produced as the result of hyperglycemia are known to stimulate the production of extracellular matrix (ECM) proteins, resulting in glomerulosclerosis. Exposure of cultured mesangial cells to AGEs results in a receptor-mediated upregulation of mRNA and protein secretion of type IV collagen (Col4), which is a major component of ECM. Here we review recent novel insights into the pathogenesis and diagnosis of DN, with a special emphasis on the emerging concept that diabetic glomerulosclerosis can result from activation of the signaling cascade leading to irreversible ECM overproduction. Finally, we describe signaling pathways involved in the initial change of DN and how these pathways can be manipulated for therapeutic benefit.
(キーワード): Animals / Biological Markers / Cells, Cultured / Collagen Type IV / Diabetic Nephropathies / Glomerular Mesangium / Glycosylation End Products, Advanced / Humans / RNA, Messenger / Signal Transduction / Smad1 Protein / Up-Regulation
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21360446; ● Search Scopus @ Elsevier (PMID): 21360446

(PubMed: 21360446) Akira Mima, Hideharu Abe, Kojiro Nagai, Hidenori Arai, Takeshi Matsubara, Makoto Araki, Kazuo Torikoshi, Tatsuya Tominaga, Noriyuki Iehara, Atsushi Fukatsu, Toru Kita and Toshio Doi :
Activation of Src mediates PDGF-induced Smad1 phosphorylation and contributes to the progression of glomerulosclerosis in glomerulonephritis.,
PLoS ONE, Vol.6, No.3, e17929, 2011.

(要約): Platelet-derived growth factor (PDGF) plays critical roles in mesangial cell (MC) proliferation in mesangial proliferative glomerulonephritis. We showed previously that Smad1 contributes to PDGF-dependent proliferation of MCs, but the mechanism by which Smad1 is activated by PDGF is not precisely known. Here we examined the role of c-Src tyrosine kinase in the proliferative change of MCs. Experimental mesangial proliferative glomerulonephritis (Thy1 GN) was induced by a single intravenous injection of anti-rat Thy-1.1 monoclonal antibody. In Thy1 GN, MC proliferation and type IV collagen (Col4) expression peaked on day 6. Immunohistochemical staining for the expression of phospho-Src (pSrc), phospho-Smad1 (pSmad1), Col4, and smooth muscle -actin (SMA) revealed that the activation of c-Src and Smad1 signals in glomeruli peaked on day 6, consistent with the peak of mesangial proliferation. When treated with PP2, a Src inhibitor, both mesangial proliferation and sclerosis were significantly reduced. PP2 administration also significantly reduced pSmad1, Col4, and SMA expression. PDGF induced Col4 synthesis in association with increased expression of pSrc and pSmad1 in cultured MCs. In addition, PP2 reduced Col4 synthesis along with decreased pSrc and pSmad1 protein expression in vitro. Moreover, the addition of siRNA against c-Src significantly reduced the phosphorylation of Smad1 and the overproduction of Col4. These results provide new evidence that the activation of Src/Smad1 signaling pathway plays a key role in the development of glomerulosclerosis in experimental glomerulonephritis.
(キーワード): Animals / Blotting, Western / Disease Progression / Glomerulonephritis / 免疫組織化学 (immunohistochemistry) / Mice / Mice, Inbred C57BL / リン酸化 (phosphorylation) / Platelet-Derived Growth Factor / Proto-Oncogene Proteins pp60(c-src) / RNA, Small Interfering / シグナル伝達 (signal transduction) / Smad1 Protein
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0017929
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21445358; ● Search Scopus @ Elsevier (PMID): 21445358; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0017929

(DOI: 10.1371/journal.pone.0017929, PubMed: 21445358) 長井幸二郎, 楠瀬賢也, 西尾進, 竹谷善雄, 山田博胤, 佐田政隆, 近藤直樹, 岸史, 岸誠司, 荒岡利和, 松浦元一, 美馬晶, 安部秀斉, 村上太一, 中村雅将, 土井俊夫 :
片腎の高齢者腎機能障害患者において超音波検査で腎動脈狭窄症を指摘され，経皮的腎血管拡張術で高血圧，腎機能の著明な改善がみられた1例,
日本腎臓学会誌, Vol.53, No.1, 68-74, 2011年.

(要約): Arteriosclerotic renal artery stenosis is one of the increasingly common diseases that affects many aged patients. There are various non-invasive methods to diagnose renal artery stenosis, such as contrast enhanced CT or MRI. However, these methods are not appropriate for patients with renal dysfunction. Ultrasound sonography is becoming one of the promising methods to diagnose artery stenosis because of photographic improvements. In this case, a 72-year-old woman was hospitalized 7 months after nephrectomy because of severe hypertension, heart failure and kidney dysfunction. The heart failure was quite uncontrollable in spite of massive administration of diuretics, and finally, hemodialysis was started to control her volume status. In consideration of her past history and abdominal bruit, we evaluated the renal artery stenosis by ultrasound sonography and confirmed the diagnosis by renal angiography. To improve hypertension control, we performed renal artery stenting, which resulted in an impressive improvement of her blood pressure and renal function. We recognized the importance of careful causal evaluation of renal dysfunction, even though it is difficult to apply invasive therapy to patients after nephrectomy.
(キーワード): Aged / Female / Heart Failure / Humans / Hypertension / Nephrectomy / Renal Artery Obstruction / Renal Insufficiency / Stents / Treatment Outcome
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21370580; ● CiNii @ 国立情報学研究所 (CRID): 1571980074923138304; ● Search Scopus @ Elsevier (PMID): 21370580

(PubMed: 21370580, CiNii: 1571980074923138304) Taichi Murakami, Hideharu Abe, Kojiro Nagai, Tatsuya Tominaga, Norimichi Takamatsu, Toshikazu Araoka, Seiji Kishi, Toshikazu Takahashi, Akira Mima, Yoshimi Takai, Jeffrey B. Kopp and Toshio Doi :
Trophoblast glycoprotein: possible candidate mediating podocyte injuries in glomerulonephritis.,
American Journal of Nephrology, Vol.32, No.6, 505-521, 2010.

(要約): trophoblast glycoprotein (Tpbg), a 72-kDa transmembrane glycoprotein, is known to regulate the phenotypes of epithelial cells by modifying actin organization and cell motility. Recently, a microarray study showed that Tpbg is upregulated in Thy1 glomerulonephritis (Thy1 GN). We hypothesized that Tpbg regulates cytoskeletal rearrangement and modulates phenotypic alteration in podocytes under pathological conditions.
(キーワード): 分散分析 (analysis of variance) / Animals / Cells, Cultured / Focal Adhesions / Glomerulonephritis, Membranoproliferative / Isoantibodies / Kidney Glomerulus / Male / Membrane Glycoproteins / Mice / Models, Animal / Podocytes / RNA, Messenger / Rats / Rats, Wistar / Statistics, Nonparametric / Stress Fibers / Transfection / Transforming Growth Factor beta / Up-Regulation
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000321366
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20980737; ● Summary page in Scopus @ Elsevier: 2-s2.0-77958492409

(DOI: 10.1159/000321366, PubMed: 20980737, Elsevier: Scopus) Toshikazu Araoka, Hiroya Takeoka, Keisuke Nishioka, Masaki Ikeda, Makiko Kondo, Azusa Hoshina, Seiji Kishi, Makoto Araki, Rokuro Mimura, Taichi Murakami, Akira Mima, Kojiro Nagai, Hideharu Abe and Toshio Doi :
Successful management of refractory pleural effusion due to systemic immunoglobulin light chain amyloidosis by vincristine adriamycin dexamethasone chemotherapy: a case report.,
Journal of Medical Case Reports, Vol.4, 322, 2010.

(出版サイトへのリンク): ● Publication site (DOI): 10.1186/1752-1947-4-322
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20955545; ● Search Scopus @ Elsevier (PMID): 20955545; ● Search Scopus @ Elsevier (DOI): 10.1186/1752-1947-4-322

(DOI: 10.1186/1752-1947-4-322, PubMed: 20955545) Toshikazu Araoka, Hideharu Abe, Tatsuya Tominaga, Akira Mima, Takeshi Matsubara, Taichi Murakami, Seiji Kishi, Kojiro Nagai and Toshio Doi :
Transcription factor 7-like 2 (TCF7L2) regulates activin receptor-like kinase 1 (ALK1)/Smad1 pathway for development of diabetic nephropathy.,
Molecules and Cells, Vol.30, No.3, 209-218, 2010.

(要約): Smad1 has previously been shown to play a key role in the development of diabetic nephropathy (DN), by increasing synthesis of extracellular matrix. However, the regulatory mechanism of Smad1 in DN is still unclear. This study aims to elucidate molecular interactions between activin receptor-like kinase 1 (ALK1)/Smad1 signaling pathway and transcription factor 7-like 2 (TCF7L2) in the progression of DN in vitro and in vivo. The expressions of TCF7L2 and ALK1 were induced by advanced glycation end products (AGEs) in parallel with Smad1, phosphorylated Smad1 (pSmad1), and alpha-smooth muscle actin (-SMA) through TGF-1 in cultured mesangial cells. Constitutively active ALK1 increased pSmad1 and -SMA expressions. The binding of TCF7L2 to ALK1 promoter was confirmed by chromatin immunoprecipitation assay. Furthermore, TCF7L2 induced promoter activity of ALK1. AGEs and TGF-1 induced a marked increase in TCF7L2 expression in parallel with ALK1. Overexpression of TCF7L2 increased the expressions of ALK1 and Smad1. Inversely, TCF7L2 knockdown by siRNA suppressed -SMA expression as well as ALK1 and Smad1. The iNOS transgenic mice (iNOS-Tgm), which developed diabetic glomerulosclerosis resembling human diabetic nephropathy, exhibited markedly increased expressions of ALK1, TCF7L2, Smad1, pSmad1, and -SMA in glomeruli in association with mesangial matrix expansion. These results provide a new evidence that the TCF7L2/ALK1/Smad1 pathway plays a key role in the development of DN.
(キーワード): Activin Receptors, Type II / Animals / Cells, Cultured / Diabetic Nephropathies / Disease Progression / Glomerular Mesangium / Humans / Mesangial Cells / Mice / Mice, Transgenic / Nitric Oxide Synthase Type II / Protein Binding / RNA, Small Interfering / シグナル伝達 (signal transduction) / Smad1 Protein / Transcription Factor 7-Like 2 Protein / Transcriptional Activation / Transgenes
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10059-010-0109-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20803090; ● Summary page in Scopus @ Elsevier: 2-s2.0-78049255269

(DOI: 10.1007/s10059-010-0109-9, PubMed: 20803090, Elsevier: Scopus) Toshikazu Araoka, Hiroya Takeoka, Hideharu Abe, Seiji Kishi, Makoto Araki, Keisuke Nishioka, Masaki Ikeda, Tetsuro Mazaki, Shiori Ikemura, Makiko Kondo, Azusa Hoshina, Kojiro Nagai, Akira Mima, Taichi Murakami, Rokuro Mimura, Kazumasa Oka, Takao Saito and Toshio Doi :
Early diagnosis and treatment may prevent the development of complications in an adult patient with glycogen storage disease type Ia.,
Internal Medicine, Vol.49, No.16, 1787-1792, 2010.

(要約): Type Iota(a) glycogen storage disease (GSD Iota(a)) is caused by the deficiency of glucose-6-phosphatase activity, which results in metabolic disorder and organ failure, including renal failure. GSD Iota(a) patients are generally diagnosed at a median age of 6 months. However, we report a 20-year-old Japanese female with newly diagnosed GSD Iota(a) . The renal disorder of GSD Iota(a) is considered to be produced by glomerular hyperfiltration, TGF-beta expression which is induced by renin-angiotensin-aldosterone system (RAS) and uric acid, and the increase in both small dense LDL and modified LDL which is characteristic of GSD Iota(a) as well as hypertriglyceridemia. With the administration of intensive therapies, including angiotensin type 1-receptor blocker and some lipid lowering drugs, along with traditional dietary therapy, daily proteinuria of the patient improved from 2.1 g to 0.78 g. Although the patients of GSD Iota(a) should receive an early and accurate diagnosis and effective therapies before the age of 1 year, the combination of traditional dietary therapies and intensive therapies may have therapeutic potential for the complications of adult patients. In this report, we describe the management of renal disease and the characteristic features of this metabolic disorder.
(キーワード): Early Diagnosis / Female / Glycogen Storage Disease Type I / Humans / Kidney Diseases / Kidney Glomerulus / Treatment Outcome / Young Adult
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.49.3425
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20720360; ● Summary page in Scopus @ Elsevier: 2-s2.0-77956219921

(DOI: 10.2169/internalmedicine.49.3425, PubMed: 20720360, Elsevier: Scopus) A Mima, N Iehara, T Matsubara, S Yamamoto, Hideharu Abe, Kojiro Nagai, M Matsuura, T Murakami, S Kishi, T Araoka, F Kishi, N Kondo, R Shigeta, K Yoshikawa, T Takahashi, T Kita, Toshio Doi and A Fukatsu :
Successful treatment of membranoproliferative glomerulonephritis associated with hepatitis B and C virus simultaneous infection patient.,
Clinical Nephrology, Vol.73, No.2, 167-169, 2010.

(キーワード): Antiviral Agents / Biopsy / Drug Therapy, Combination / Female / Follow-Up Studies / Glomerulonephritis, Membranoproliferative / Hepacivirus / Hepatitis B / Hepatitis B virus / Hepatitis C / Humans / Interferon-alpha / Microscopy, Fluorescence / Middle Aged / RNA, Viral / Ribavirin
(出版サイトへのリンク): ● Publication site (DOI): 10.5414/CNP73167
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20129026; ● Search Scopus @ Elsevier (PMID): 20129026; ● Search Scopus @ Elsevier (DOI): 10.5414/CNP73167

(DOI: 10.5414/CNP73167, PubMed: 20129026) Norimichi Takamatsu, Hideharu Abe, Tatsuya Tominaga, Kunihiko Nakahara, Yumi Ito, Yoko Okumoto, Jiyoong Kim, Masafumi Kitakaze and Toshio Doi :
Risk factors for chronic kidney disease in Japan: a community-based study.,
BMC Nephrology, Vol.10, 34, 2009.

(要約): Chronic kidney disease (CKD) is increasingly being recognized as a predictor for both end-stage renal disease and cardiovascular disease. The present study, conducted on individuals from a community in Arita, Japan, was designed to evaluate biomarkers that can be used to determine the associated factors for CKD.
(キーワード): Adult / Aged / Aged, 80 and over / Cross-Sectional Studies / Female / Glomerular Filtration Rate / Humans / 日本 (Japan) / Kidney Failure, Chronic / Male / Middle Aged / Residence Characteristics / Risk Factors / Young Adult
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/1471-2369-10-34
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19860890; ● Search Scopus @ Elsevier (PMID): 19860890; ● Search Scopus @ Elsevier (DOI): 10.1186/1471-2369-10-34

(DOI: 10.1186/1471-2369-10-34, PubMed: 19860890) 荒岡利和, 竹岡浩也, 西岡敬祐, 岸誠司, 荒木真, 岸史, 繁田令子, 村上太一, 近藤直樹, 松浦元一, 吉川和寛, 美馬晶, 長井幸二郎, 高橋利和, 安部秀斉, 池田昌樹, 近藤麻紀子, 杉山あずさ, 菅野雅彦, 土井俊夫 :
C型慢性肝炎合併維持血液透析患者に対する安全かつ効果的なインターフェロン-β治療法の検討,
日本透析医学会雑誌, Vol.42, No.5, 393-402, 2009年.

(要約): 維持血液透析患者のC型肝炎ウイルス(HCV)感染率が高いことは知られており，最近HCV感染が予後規定因子であるといわれている．しかし未だ血液透析患者における安全で効果的なインターフェロン(IFN)投与法は確立されていない．維持血液透析患者2名に副作用が少ないIFN-βを中長期間(24週，2年)投与し，薬物動態，投与法，安全性，治療効果について検討した．1例目は38歳男性，高ウイルス1型．初回2週間連日点滴静注し以降は透析日のみ投与した．透析日は内シャント静脈ラインから透析開始直前30分でIFN-β 600万単位を投与した．早期ウイルス学的陰性になったが治療後ウイルスの再増加がありIFN-βを再投与した．再治療は1週間連日点滴静注し以降は透析日のみ投与した．投与法を透析開始直後30分に変更し血液透析回路から投与した．2年間投与で特に副作用もなくHCV-RNA定性検査陰性となったが，持続ウイルス学的陰性は得られなかった．開始直後30分投与のCmaxは262±41 pg/mLと開始直前30分投与のCmax 214.7±38.25 pg/mLよりやや高いが透析中の約4時間で体内から消失し蓄積はなかった．2例目は58歳男性，低ウイルス量2型．1例目再治療時に準じてIFN-βを透析開始直後30分で24週間投与し持続ウイルス学的陰性を得た．血圧低下にIFN-βの関与を疑い8週目から300万単位に減量し改善した．Cmaxは600万単位投与で259±43.9 pg/mL．300万単位投与で143.5±5.09 pg/mL．ほかの副作用はなかった．IFN-α製剤は副作用のため治療継続，長期投与が困難であるがIFN-βはそれを可能にする．血液透析開始直後30分投与は安全面，治療効果において優れた投与法である．
(キーワード): 長期投与 / 薬物動態 / 血液透析患者 / インターフェロン-β / C型慢性肝炎 / chronic administration / drug kinetics / patient with receiving hemodialysis / interferon-beta / chronic hepatitis C
(出版サイトへのリンク): ● Publication site (DOI): 10.4009/jsdt.42.393
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390282679656191872; ● Search Scopus @ Elsevier (DOI): 10.4009/jsdt.42.393

(DOI: 10.4009/jsdt.42.393, CiNii: 1390282679656191872) Akira Mima, Masanao Toma, Takeshi Matsubara, Fumihiko Shiota, Noriyuki Iehara, Hideharu Abe, Kojiro Nagai, Toshikazu Takahashi, Motokazu Matsuura, Taichi Murakami, Seiji Kishi, Toshikazu Araoka, Fumi Kishi, Naoki Kondo, Reiko Shigeta, Kazuhiro Yoshikawa, Takeshi Kimura, Toru Kita, Toshio Doi and Atsushi Fukatsu :
Angio-embolization of renal artery pseudoaneurysm after renal biopsy: a case report.,
Renal Failure, Vol.31, No.8, 753-755, 2009.

(要約): Renal artery pseudoaneurysm is a rare clinical entity that has been reported after renal biopsy, percutaneous renal surgery, penetrating trauma, and rarely blunt renal trauma. We present the case of a 37-year-old man with ruptured renal artery pseudoaneurysm accompanied by massive gross hematuria, urinary clot retention, and bladder tamponade, which were the presenting signs seven hours after renal biopsy. Abdominal CT scan showed a large perinephric, intracapsular hematoma of left kidney. His angiogram revealed a left renal segmental artery pseudoaneurysm that measured 1 cm x 1 cm. He was successfully treated by selective embolization of the arterial branch supplying the pseudoaneurysm.
(キーワード): Adult / Aneurysm, False / Aneurysm, Ruptured / Biopsy / Embolization, Therapeutic / Humans / Kidney / Kidney Diseases / Male / Renal Artery / Scleroderma, Systemic
(出版サイトへのリンク): ● Publication site (DOI): 10.3109/08860220903125298
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19814646; ● Summary page in Scopus @ Elsevier: 2-s2.0-70350666279

(DOI: 10.3109/08860220903125298, PubMed: 19814646, Elsevier: Scopus) Toshio Doi, Akira Mima, Takeshi Matsubara, Tatsuya Tominaga, Hidenori Arai and Hideharu Abe :
The current clinical problems for early phase of diabetic nephropathy and approach for pathogenesis of diabetic nephropathy.,
Diabetes Research and Clinical Practice, Vol.82, No.Suppl 1, S21-4, 2008.

(要約): The important clinical problems of diabetic nephropathy are both proteinuria and decrease of renal function. Pathological analysis showed decrease of GFR was correlated to degree of mesangial expansion but not thickening of GBM nor the other findings in human type 1 diabetic nephropathy. From the perspective in renal dysfunction, mesangial matrix expansion was crucial for diabetic nephropathy. However, there was no difference of mesangial expansion between normal and microalbuminuria stage in type 1 and 2 diabetes mellitus (DM). On the other hand, microalbuminuria definitely shows a key related factor for cardiovascular events, but it does not indicate a clear interaction for glomerulosclerosis. We need to search a new clinical marker for renal injury. We have first shown that Smad1 is a transcription factor for alpha1 and 2 of type 4 collagen (Col4), which is a major component of glomerulosclerosis. We have also identified Smad1 is a critical responsible molecule for developing glomerulosclerosis in rat diabetic nephropathy. We have found the good correlation between glomerulosclerosis and urinary Smad1 but not between glomerulosclerosis and urine albumin. These data suggests that urine Smad1 is a promising clinical marker for underlying glomerular damages in early stage diabetic nephropathy. The study also implicates that angiotensin II (AngII)-Src-Smad1 signaling pathway has played a key role for development of diabetic nephropathy. These suggest that it is necessary to clarify the whole mechanism related to Smad1 to identify the pathogenesis of diabetic nephropathy.
(キーワード): Animals / 動脈硬化 (atherosclerosis) / Biological Markers / Diabetic Nephropathies / Disease Models, Animal / Glomerular Mesangium / Kidney Glomerulus / Mesangial Cells / Rats / Smad1 Protein
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.diabres.2008.09.013
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18842318; ● Search Scopus @ Elsevier (PMID): 18842318; ● Search Scopus @ Elsevier (DOI): 10.1016/j.diabres.2008.09.013

(DOI: 10.1016/j.diabres.2008.09.013, PubMed: 18842318) Akira Mima, Hidenori Arai, Takeshi Matsubara, Hideharu Abe, Kojiro Nagai, Yukinori Tamura, Kazuo Torikoshi, Makoto Araki, Hiroshi Kanamori, Toshikazu Takahashi, Tatsuya Tominaga, Motokazu Matsuura, Noriyuki Iehara, Atsushi Fukatsu, Toru Kita and Toshio Doi :
Urinary Smad1 is a novel marker to predict later onset of mesangial matrix expansion in diabetic nephropathy.,
Diabetes, Vol.57, No.6, 1712-1722, 2008.

(要約): We reported that Smad1 is a key transcriptional factor for mesangial matrix expansion in diabetic nephropathy. In this study, we examined whether urinary Smad1 in an early phase of diabetes can predict later development of glomerulosclerosis in diabetic nephropathy and how an angiotensin II type 1 receptor blocker (ARB) can modulate structural changes and urinary markers.
(キーワード): Angiotensin II Type 1 Receptor Blockers / Animals / Biological Markers / Diabetes Mellitus, Experimental / Diabetic Nephropathies / Glomerular Mesangium / Imidazoles / Kidney / Male / Mice / Mice, Inbred C57BL / Rats / Rats, Sprague-Dawley / Smad1 Protein / Tetrazoles
(出版サイトへのリンク): ● Publication site (DOI): 10.2337/db07-1726
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18285555; ● Search Scopus @ Elsevier (PMID): 18285555; ● Search Scopus @ Elsevier (DOI): 10.2337/db07-1726

(DOI: 10.2337/db07-1726, PubMed: 18285555) Akira Mima, Takeshi Matsubara, Hidenori Arai, Hideharu Abe, Kojiro Nagai, Hiroshi Kanamori, Eriko Sumi, Toshikazu Takahashi, Noriyuki Iehara, Atsushi Fukatsu, Toru Kita and Toshio Doi :
Angiotensin II-dependent Src and Smad1 signaling pathway is crucial for the development of diabetic nephropathy.,
Laboratory Investigation; a Journal of Technical Methods and Pathology, Vol.86, No.9, 927-939, 2006.

(要約): Angiotensin II (Ang II) is known to play a pivotal role in the development of diabetic nephropathy. However, the precise mechanism of Ang II-mediated effects on diabetic nephropathy is still unknown. We have reported that Smad1 plays a key role in diabetic mesangial matrix expansion and directly regulates the transcription of type IV collagen (Col4) in vitro and in vivo. Here we examined the effect of Ang II on the expression of Smad1 and mesangial matrix expansion in streptozotocin (STZ)-induced diabetic rats in vivo, using Ang II type 1 receptor blocker, olmesartan. We also examined the signaling mechanism by which Ang II induces mesangial matrix expansion in vitro. Treatment of diabetic rats with low-dose olmesartan for 20 weeks reduced albuminuria and hyperfiltration without affecting blood pressure and inhibited mesangial matrix expansive changes and the expression of Col4 and smooth muscle alpha actin compared with those in untreated rats. Immunohistochemical staining and Western blotting showed that the increased expression of Smad1, phospho-Smad1, and phospho-Src was inhibited by olmesartan. Ang II induced Col4 synthesis and increased expression of phospho-Src and phospho-Smad1 in cultured mesangial cells, which was blocked by olmesartan. PP2, a Src tyrosine kinase inhibitor, and overexpression of dominant negative Src also reduced the phosphorylation of Smad1. Moreover, addition of small-interfering RNA against Src significantly reduced the phosphorylation of Smad1 and synthesis of Col4. Taken together, these results indicate that Ang II can regulate the development of mesangial matrix expansion in the early phase of diabetic nephropathy through Src and Smad1.
(キーワード): Angiotensin II / Angiotensin II Type 1 Receptor Blockers / Animals / Butadienes / Cell Line / Collagen Type IV / Diabetes Mellitus, Experimental / Diabetic Nephropathies / 遺伝子発現 (gene expression) / Glomerular Mesangium / Imidazoles / Male / Mesangial Cells / Nitriles / リン酸化 (phosphorylation) / Pyrimidines / RNA, Small Interfering / Rats / Rats, Sprague-Dawley / シグナル伝達 (signal transduction) / Smad1 Protein / Tetrazoles / src-Family Kinases
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/labinvest.3700445
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16767106; ● Search Scopus @ Elsevier (PMID): 16767106; ● Search Scopus @ Elsevier (DOI): 10.1038/labinvest.3700445

(DOI: 10.1038/labinvest.3700445, PubMed: 16767106) Takeshi Matsubara, Hideharu Abe, Hidenori Arai, Kojiro Nagai, Akira Mima, Hiroshi Kanamori, Eriko Sumi, Toshikazu Takahashi, Motokazu Matsuura, Noriyuki Iehara, Atsushi Fukatsu, Toru Kita and Toshio Doi :
Expression of Smad1 is directly associated with mesangial matrix expansion in rat diabetic nephropathy.,
Laboratory Investigation; a Journal of Technical Methods and Pathology, Vol.86, No.4, 357-368, 2006.

(要約): Diabetic nephropathy is the leading cause of end-stage renal disease, and glomerular mesangial matrix expansion is the hallmark in diabetic nephropathy. However, the precise mechanism for the development of mesangial matrix expansion has remained unknown. The key component involved in mesangial matrix expansion is type IV collagen (Col4). Recently, we have reported that Smad1 transcriptionally regulates expression of Col4 under diabetic conditions in vitro. Here we show that this direct regulator of Col4 also plays a crucial role for mesangial matrix expansion in vivo. Streptozotocin-induced diabetic rats are the model of incipient diabetic nephropathy, and showed various levels of mesangial matrix expansion at 24 weeks. The glomerular expression of Smad1 was significantly increased in diabetic rats with more mesangial matrix expansion by Western blot and immunohistochemical analysis. Furthermore, the glomerular expression of Smad1 was closely correlated with the glomerular expression of Col4 and smooth muscle alpha actin (alpha-SMA), while albuminuria or glomerular filtration rate was not correlated with mesangial matrix expansion. We also found that urinary excretion of Smad1 was closely associated with the severity of mesangial matrix expansion. In cultured mesangial cells expression of Smad1 upregulated the transcriptional activity of key molecules in mesangial matrix expansion, such as Col4 and alpha-SMA. These data indicate the critical involvement of Smad1 in mesangial matrix expansion in the early phase of diabetic nephropathy. Our data imply that urinary Smad1 might be a representative diagnostic marker for mesangial matrix expansion in diabetic nephropathy.
(キーワード): Actins / Animals / Cells, Cultured / Collagen Type IV / Diabetes Mellitus, Experimental / Diabetic Nephropathies / 遺伝子発現 (gene expression) / Glomerular Mesangium / Kidney Failure, Chronic / Kidney Glomerulus / Male / Mesangial Cells / リン酸化 (phosphorylation) / Rats / Rats, Sprague-Dawley / Smad1 Protein
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/labinvest.3700400
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16482100; ● Search Scopus @ Elsevier (PMID): 16482100; ● Search Scopus @ Elsevier (DOI): 10.1038/labinvest.3700400

(DOI: 10.1038/labinvest.3700400, PubMed: 16482100) Toshikazu Takahashi, Hideharu Abe, Hidenori Arai, Takeshi Matsubara, Kojiro Nagai, Motokazu Matsuura, Noriyuki Iehara, Masayuki Yokode, Shinichi Nishikawa, Toru Kita and Toshio Doi :
Activation of STAT3/Smad1 is a key signaling pathway for progression to glomerulosclerosis in experimental glomerulonephritis.,
The Journal of Biological Chemistry, Vol.280, No.8, 7100-7106, 2004.

(要約): Mesangial cell proliferation is a significant event in the development of progressive glomerular injuries. However, the issue of how cell proliferation is involved in the development of glomerulosclerosis is unclear. Recently, we showed that the overexpression of type IV collagen (Col IV), a major component of mesangial extracellular matrix, is transcriptionally regulated by Smad1 in diabetic glomerulosclerosis. In this study, we have demonstrated the effect of the administration of an anti-platelet-derived growth factor (PDGF) beta-receptor antibody (APB5) blocking activation by the PDGF-B chain on rat glomerulonephritis and have examined the signaling pathways that regulate both glomerular cell proliferation and glomerulosclerosis in vivo and in vitro. Experimental mesangial proliferative glomerulonephritis (Thy1 GN) was induced by a single intravenous injection of anti-rat Thy-1.1 monoclonal antibody. In Thy1 GN, mesangial cell proliferation and the expression of Col IV peaked at day 6. Immunohistochemical staining for the expression of Smad1, phospho-Smad1 (pSmad1), and phospho-STAT3 (pSTAT3) revealed that the peak for glomerular Smad1 expression occurred at day 6, consistent with the peak for mesangial proliferation. The expression of pSmad1 was up-regulated at day 1, and the peak for glomerular pSmad1 expression occurred at day 4 of the disease. When treated with APB5, both mesangial proliferation and sclerosis were reduced significantly. The expression of Smad1, pSmad1, and pSTAT3 was also significantly reduced by the administration of APB5. PDGF induced both mesangial cell replication and Col IV synthesis in association with an increased expression of pSTAT3 and pSmad1 on cultured mesangial cells. In addition, APB5 reduced mesangial cell proliferation in association with decreased pSmad1, pSTAT3, and Col IV protein expressions in vitro. The introduction of dominant negative STAT3 significantly decreased the expression of Col IV in cultured mesangial cells. These data suggest that the activation of STAT3 and Smad1 participates in the developing process of glomerulosclerosis in experimental glomerulonephritis.
(キーワード): Animals / Antibodies, Monoclonal / Cell Proliferation / Collagen Type IV / DNA-Binding Proteins / Disease Models, Animal / Disease Progression / Gene Expression Regulation / Glomerular Mesangium / Glomerulonephritis / Glomerulosclerosis, Focal Segmental / Male / Phosphoproteins / Proto-Oncogene Proteins c-sis / Rats / Rats, Wistar / STAT3 Transcription Factor / Signal Transduction / Smad Proteins / Smad1 Protein / Trans-Activators
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M411064200
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15591053; ● Search Scopus @ Elsevier (PMID): 15591053; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M411064200

(DOI: 10.1074/jbc.M411064200, PubMed: 15591053) Seiji Ohashi, Hideharu Abe, Toshikazu Takahashi, Yasuhiko Yamamoto, Masayoshi Takeuchi, Hidenori Arai, Kazuhiro Nagata, Toru Kita, Hiroshi Okamoto, Hiroshi Yamamoto and Toshio Doi :
Advanced glycation end products increase collagen-specific chaperone protein in mouse diabetic nephropathy,
The Journal of Biological Chemistry, Vol.279, No.19, 19816-19823, 2004.

(要約): Advanced glycation end products (AGEs) appear to contribute to the diabetic complications. This study reports the inhibitory effect of OPB-9195 (OPB), an inhibitor of AGEs formation, and the role of a collagen-specific molecular chaperone, a 47-kDa heat shock protein (HSP47) in diabetic nephropathy. Transgenic mice carrying nitric-oxide synthase cDNA fused with insulin promoter (iNOSTg) leads to diabetes mellitus. The iNOSTg mice at 6 months of age represented diffuse glomerulosclerosis, and the expression of HSP47 was markedly increased in the mesangial area in parallel with increased expression of types I and IV collagens. OPB treatment ameliorated glomerulosclerosis in the iNOSTg mice associated with the decreased expression of HSP47 and types I and IV collagens. The expression of transforming growth factor-beta (TGF-beta) was increased in glomeruli of iNOSTg mice and decreased after treatment with OPB. To confirm these mechanisms, cultured mesangial cells were stimulated with AGEs. AGEs significantly increased the expression of HSP47, type IV collagen, and TGF-beta mRNA. Neutralizing antibody for TGF-beta inhibited the overexpression of both HSP47 and type IV collagen in vitro. In conclusion, AGEs increase the expression of HSP47 in association with collagens, both in vivo and in vitro. The processes may be mediated by TGF-beta.
(キーワード): Animals / Blood Glucose / Blotting, Western / Cells, Cultured / コラーゲン (collagen) / DNA-Binding Proteins / Diabetic Nephropathies / Glomerular Mesangium / Glycosylation End Products, Advanced / HSP47 Heat-Shock Proteins / Heat-Shock Proteins / インスリン (insulin) / Kidney / Lasers / Male / Mice / Mice, Inbred C57BL / Mice, Transgenic / Microscopy, Fluorescence / Oligonucleotides, Antisense / Polymerase Chain Reaction / Promoter Regions, Genetic / RNA, Messenger / RNA, Small Interfering / Ribonucleases / Smad Proteins / Thiadiazoles / Thiazolidines / Time Factors / Trans-Activators / Transfection / Transforming Growth Factor beta
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M310428200
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15004023; ● CiNii @ 国立情報学研究所 (CRID): 1570572701785650688; ● Search Scopus @ Elsevier (PMID): 15004023; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M310428200

(DOI: 10.1074/jbc.M310428200, PubMed: 15004023, CiNii: 1570572701785650688) Hideharu Abe, Takeshi Matsubara, Noriyuki Iehara, Kojiro Nagai, Toshikazu Takahashi, Hidenori Arai, Toru Kita and Toshio Doi :
Type IV collagen is transcriptionally regulated by Smad1 under advanced glycation end-products (AGEs) stimulation,
The Journal of Biological Chemistry, Vol.279, No.14, 14201-14206, 2004.

(要約): Prolonged exposure to hyperglycemia is now recognized as the most significant causal factor of diabetic complications. Excessive advanced glycation end products (AGEs) as a result of hyperglycemia in tissues or in the circulation may critically affect the progression of diabetic nephropathy. In diabetic nephropathy, glomerulosclerosis is a typical pathologic feature characterized by the increase of the extracellular matrix (ECM). We have reported previously that alpha1 type IV collagen (Col4) is one of the major components of ECM, which is up-regulated by AGEs, and that the overexpression of Col4 is transcriptionally regulated by an unknown transcription factor binding to the promoter. Here we identified this protein as Smad1 by yeast one-hybrid screening. Using chromatin immunoprecipitation and reporter assay, we observed that Smad1 directly regulated transcription for Col4 through the binding of Smad1 to the promoter of Col4. Smad1 was significantly induced along with Col4 in AGE-treated mesangial cells. Moreover, suppression of Smad1 by antisense morpholino resulted in a decrease of AGE-induced Col4 overproduction. To elucidate the interaction between transforming growth factor-beta and Smad1, we investigated whether activin receptor-liked kinase1 (ALK1) was involved in this regulation. AGE stimulation significantly increased the expression of the ALK1 mRNA in mesangial cells. We also demonstrated that Smad1 and ALK1 were highly expressed in human diabetic nephropathy. These results suggest that the modulation of Smad1 expression is responsible for the initiation and progression of diabetic nephropathy and that blocking Smad1 signaling may be beneficial in preventing diabetic nephropathy and other various diabetic complications.
(キーワード): Activin Receptors, Type I / Activin Receptors, Type II / Animals / Cell Line / Collagen Type IV / DNA-Binding Proteins / Diabetic Nephropathies / Extracellular Matrix Proteins / Gene Library / Glomerular Mesangium / Glycosylation End Products, Advanced / Humans / Mice / Mice, Inbred C57BL / Promoter Regions, Genetic / Smad Proteins / Smad1 Protein / Trans-Activators / Transcription, Genetic / Two-Hybrid System Techniques
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M310427200
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14732718; ● Search Scopus @ Elsevier (PMID): 14732718; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M310427200

(DOI: 10.1074/jbc.M310427200, PubMed: 14732718)

MISC

安部秀斉 :
interview 研究の窓辺,
血圧, Vol.17, No.4, 12-15, 2010年.

総説・解説: 安部秀斉 :
糖尿病性腎症の分子病態解明と修復治療法の開発,
細胞, Vol.49, No.10, 26,27, 2017年5月. 安部秀斉 :
CKD(慢性腎臓病),
歯界展望, 81-82, 2014年5月. 安部秀斉, 土井俊夫 :
尿沈渣検査の将来--現在の限界とその克服への試み--,
臨床検査, Vol.58, No.10, 1177, 2014年. 安部秀斉 :
心腎貧血連関における心血管イベント予測新規バイオマーカー血中Smad1の解析,
腎臓, Vol.34, No.2, 112-116, 2011年7月. 安部秀斉 :
腎疾患の病態形成におけるBMP4・Smad1の役割,
Annual Review腎臓2011, 59-66, 2011年4月. 荒岡利和, 安部秀斉, 長井幸二郎, 美馬晶, 冨永辰也, 松浦元一, 村上太一, 岸誠司, 繁田令子, 岸史, 吉川和寛, 土井俊夫 :
2型糖尿病原因遺伝子TCF7L2を介した糖尿病性腎症感受性遺伝子ALK1の分子調節機構の解析,
Diabetes Frontier, Vol.21, No.5, 614, 2010年10月.
講演・発表: Masanori Tamaki, Tatsuya Tominaga, Yui Fujita, Taichi Murakami, Seiji Kishi, Hideharu Abe, Kojiro Nagai and Toshio Doi :
A Novel All-Trans Retinoic Acid Therapy Directly Suppresses Bone Morphogenetic Protein 4 in Mouse Diabetic Nephropathy,
KIDNEY WEEK 2019 American Society of Nephrology, Nov. 2019. Kenji Nishimura, Seiji Kishi, Arisa Ochi, Hiroyuki Ono, Masanori Tamaki, Taichi Murakami, Hideharu Abe, Kenichi Aihara and Kojiro Nagai :
Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and aging after injury,
KIDNEY WEEK 2019 American Society of Nephrology, Nov. 2019. Masanori Tamaki, Taizo Inagaki, Masanori Minato, Fumi Kishi, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi :
A case of Helicobacter cinaedi-induced PD-related peritonitis detected by blood culture,
APCM-ISPD2019, Sep. 2019. 岸誠司, 西村賢二, 小野広幸, 田蒔昌憲, 岸史, 村上太一, 安部秀斉, 長井幸二郎 :
ENHANCED KIDNEY FIBROSIS AND AGING AFTER UUO IN ENOS/APOE DOUBLE KNOCKOUT MOUSE,
56th ERA-EDTA Congress, 2019年6月. Maho Iwaki, Seiji Kishi, Masanori Minato, Masanori Tamaki, Fumi Kishi, Taichi Murakami, Hideharu Abe and Kojiro Nagai :
Glomerular Injury Related to Immune Related Adverse Events: IgA Nephropathy After Nivolumab Therapy for Postoperative Recurrence of Lung Cancer,
ASN Kidney week 2018, San Diego, Oct. 2018. Masanori Tamaki, Tatsuya Tominaga, Yui Fujita, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi :
Mesangial Matrix Expansion Attenuated by All-Trans Retinoic Acid Through Direct Suppression of Bone Morphogenetic Protein 4 in Mouse Diabetic Nephropathy,
KIDNEY WEEK 2018 American Society of Nephrology, Oct. 2018. Yui Fujita, Tatsuya Tominaga, Masanori Tamaki, Taichi Murakami, Seiji Kishi, Kojiro Nagai, Hideharu Abe and Toshio Doi :
Palovarotene, Selective Retinoic Receptor- Agonist, Inhibited Both BMP4 and TGF- Signaling Pathways in Diabetic Nephropathy,
KIDNEY WEEK 2017 American Society of Nephrology, Nov. 2017. Masanori Tamaki, Tatsuya Tominaga, Yui Fujita, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi :
Glomerulosclerosis Attenuated by Retinoic Acid through Bone Morphogenetic Protein 4 Suppression in Mice with Streptozotocin-Induced Diabetes,
KIDNEY WEEK 2017 American Society of Nephrology, Nov. 2017. 村上太一, 岸誠司, 土井俊夫, 安部秀斉, 長井幸二郎 :
過粘稠症候群に血漿交換が奏功した原発性マクログロブリン血症の一例,
第62回日本透析医学会学術集会・総会, 2017年6月. Hiroyuki Ono, Seiji Kishi, Kojiro Nagai, Taichi Murakami, Hideharu Abe and Toshio Doi :
Shunt Nephritis And Pyogenic Spondylitis With A Positive PR3-ANCA Associated With Chronically Infected Ventriculo-Arterial Shunt,
the ASN Kidney Week 2016 Annual Meeting, November 15-20 in Chicago, IL., Nov. 2016. Kojiro Nagai, Tatsuya Tominaga, Taichi Murakami, Eriko Shibata, Seiji Kishi, Motokazu Matsuura, Hideharu Abe and Toshio Doi :
In vivo evidence of mTORC1-S6 kinase pathway involvement in the development of glomerulosclerosis in human IgA nephropathy,
KIDNEY WEEK 2016 American Society of Nephrology, Nov. 2016. HIroyuki Ono, Seiji Kishi, Kojiro Nagai, Taichi Murakami, Hideharu Abe and Toshio Doi :
Shunt Nephritis And Pyogenic Spondylitis With A Positive PR3-ANCA Associated With Chronically Infected Ventriculo-Arterial Shunt,
the ASN Kidney Week 2016 Annual Meeting, November 15-20 in Chicago, IL., Nov. 2016. Yui Fujita, Tatsuya Tominaga, Taichi Murakami, Seiji Kishi, Kojiro Nagai, Hideharu Abe and Toshio Doi :
The Role of BMP4 Signal Pathway on the Podocyte Injury in Diabetic Early Stage,
ASN Kidney week 2016, Nov. 2016. K Yoshikawa, Hideharu Abe, Motokazu Matsuura, Kojiro Nagai, Akira Mima, E Shibara, J Minakuchi and Toshio Doi :
High-Density Lipoprotein Cholesterol and Matrix Gla Protein Are Implicated in the Progression of Aortic Calcification through Bone Morphogenetic Protein 4- or Activin-Like Kinase 1-Induced Smad1 Activation in Patients Undergoing Maintenance Hemodialysis.,
46th American Society of Nephrology (ASN) Annual Meeting, Nov. 2013. Tatsuya Tominaga, Hideharu Abe, Kojiro Nagai, Akira Mima, Seiji Kishi, K Jishage, N Fukushima and Toshio Doi :
Role of BMP4 for regulating podocyte injury in the diabetic nephropathy.,
American Society for Cell biology, San Francisco, Dec. 2012. Hideharu Abe :
Molecular Pathogenesis of Diabetic Nephropathy,
The 10th Korea-Japan Joint Symposium on Vascular Biology, Dec. 2012. Masashi Miyoshi, Kojiro Nagai, Takei Kake, Naoshi Fukushima, Motokazu Matsuura, Eriko Shibata, Satoshi Yamada, Kazuhiro Yoshikawa, Akira Mima, Fumi Kishi, Seiji Kishi, Tatsuya Tominaga, Hideharu Abe and Toshio Doi :
Expression of Gas6 and Axl in Human IgA Nephropathy. ~A Possible Involvement of Gas6 in Podocyte Injury~,
American Society of Nephrology Kidney Week 2012, San Diego, Nov. 2012. Tatsuya Tominaga, Hideharu Abe, Kojiro Nagai, Seiji Kishi, Akira Mima and Toshio Doi :
BMP4 regulates podocyte injury in the diabetic nephropathy,
Diabetes, Philadelphia, May 2012. Seiji Kishi, Hideharu Abe, Kojiro Nagai and Toshio Doi :
SOX9 induces irreversible chondrogenic phenotypic change in diabetic nephropathy,
the 2011 Annual Meeting of the American Society for Cell Biology, Denver, Dec. 2011. Tatsuya Tominaga, Hideharu Abe, Kojiro Nagai, Seiji Kishi and Toshio Doi :
BMP4 regulates podocyte injury in the diabetic nephropathy,
The 1st Asia-Pacific Vascular Biology Meeting, Dec. 2011. Tatsuya Tominaga, Hideharu Abe, Kojiro Nagai, Seiji Kishi, Taichi Murakami and Toshio Doi :
BMP4 regulates podocyte injury in the diabetic nephropathy,
Journal of the American Society of Nephrology, Nov. 2011. 村上太一 and Hideharu Abe :
TROPHOBLAST GLYCOPROTEIN REGULATES THE PODOCYTE INJURIES IN EXPERIMENTAL GLOMERULONEPHRITIS,
World Congress of Nephrology, Vancouver, Aug. 2011. 松原雄 and Hideharu Abe :
Overexpression of Smad1 Causes Remarkable Glomerulosclerosis in Diabetic Mice.,
American Diabetes Association 69th Scientific Session, New Orleans, Jun. 2011. Seiji Kishi and Hideharu Abe :
Chondrogenic phenotypic change contributes to the irreversible progression of the diabetic nephropathy.,
50th The American Society for Cell Biology Annual Meeting, Philadelphia, Dec. 2010. 岸誠司 and Hideharu Abe :
Chondrogenic phenotypic change contributes to the irreversible progression of the diabetic nephropathy.,
50th The American Society for Cell Biology Annual Meeting, Philadelphia, Dec. 2010. 鳥越和雄 and Hideharu Abe :
PIASy Regulates SM-Actin Expression by Interacting with E12 in Mesangial Proliferative Glomerulonephritis.,
43rd American Society of Nephrology (ASN) Annual Meeting, Denver, Nov. 2010. 松原雄 and Hideharu Abe :
BMP4/Smad1 Signaling Is a Critical Therapeutic Target for Diabetic Nephropathy.,
43rd American Society of Nephrology (ASN) Annual Meeting, Denver, Nov. 2010. 荒木真 and Hideharu Abe :
Conditional Knockout of Smad1 Ameliorates Glomerulosclerosis in Progressive Glomerulonephritis.,
43rd American Society of Nephrology (ASN) Annual Meeting, Denver, Nov. 2010. Akira Mima, T Matsubara, H Arai, Hideharu Abe, N Iehara, T Kita, T Doi and A Fukatsu :
Blockade of Src/Smad1 pathway attenuates the progression of peritoneal sclerosis in a mouse experimental model,
The 12th congress of the ISPD, Istanbul, Jun. 2008. Akira Mima, H Arai, T Matsubara, Hideharu Abe, H Kanamori, E Sumi, Tatsuya Tominaga, T Takahashi, Motokazu Matsuura, N Iehara, A Fukatsu, T Kita and Toshio Doi :
Angiotensin II type I receptor blocker decreases urinary Smad1, a marker for mesangial matrix expansion in diabetic nephropathy,
2007 World Congress of Nephrology, リオデジャネイロ, Apr. 2007. 宮上慎司, 田蒔昌憲, 西村賢二, 岩城真帆, 清水郁子, 山口純代, 上田紗代, 柴田恵理子, 安部秀斉, 長井幸二郎, 𦚰野修 :
繰り返す菌血症に対し予防的抗菌薬投与が奏功した1例,
日本透析医学会雑誌, 2021年6月. 吉川珠希, 長谷栄治, 鈴木昭浩, 越智ありさ, 安部秀斉, 安井武史 :
AGE(終末糖化産物)による真皮コラーゲン繊維構造変化のSHG(第二高調波発生光)イメージング,
日本生体医工学会専門別研究会生体画像と医用人工知能研究会第3回研究会若手発表会, 2021年3月. 小笠真琴, 櫻井明子, 片岡佳子, 越智ありさ, 安部秀斉 :
ヒト尿沈渣中のCXC Chemokine Receptor遺伝子発現について,
第44回徳島県医学検査学会, 2020年12月. 吉川珠希, 長谷栄治, 鈴木昭浩, 越智ありさ, 安部秀斉, 安井武史 :
AGE(終末糖化産物)による真皮コラーゲン線維構造変化のSHG(第2高調波発生光)イメージング,
Optics & Photonics Japan 2020, 14pA3, 2020年11月. 田蒔昌憲, 湊将典, 上田紗代, 柴田恵理子, 西村賢二, 小野広幸, 小幡史明, 山本修三, 滝下佳寛, 田蒔正治, 安部秀斉, 長井幸二郎 :
急性期と慢性期ともにトシリズマブが有効であったTAFRO症候群の1例,
日本透析医学会雑誌, Vol.53, No.Suppl.1, 391, 2020年10月. 柴田恵理子, 三好雅士, 中尾隆之, 上田紗代, 西村賢二, 小野広幸, 岸史, 田蒔昌憲, 村上太一, 安部秀斉, 岸誠司, 土井俊夫, 長井幸二郎 :
プレセプシン濃度は検体処理や腎機能障害により影響をうける,
第63回日本腎臓学会学術総会, 2020年8月. 田蒔昌憲, 小野広幸, 西村賢二, 柴田恵理子, 上田紗代, 越智ありさ, 冨永辰也, 長井幸二郎, 安部秀斉 :
骨形成因子4(BMP4)はメサンギウム細胞のミトコンドリア障害を惹起する,
日本腎臓学会誌, Vol.62, No.4, 282, 2020年7月. 武村真季, 冨永辰也, 三橋英, 長井幸二郎, 安部秀斉 :
糖尿病における高タンパク食が腎臓に与える影響について②,
徳島県臨床検査技師会誌第43回徳島県医学検査学会抄録集, 2019年12月. 三橋英, 冨永辰也, 武村真季, 長井幸二郎, 安部秀斉 :
糖尿病における高タンパク食が腎臓に与える影響について①,
徳島県臨床検査技師会誌第43回徳島県医学検査学会抄録集, 2019年12月. 越智ありさ, 安部秀斉, 櫻井明子 :
iPS細胞を用いない，腎臓病治療薬HTPのための腎糸球体スフェロイド開発,
第42回日本分子生物学会年会, 2019年12月. 櫻井明子, 越智ありさ, 安部秀斉 :
ポドサイト障害における尿中バイオマーカーWT1・CXCR4による各種腎疾患の評価,
第66回日本臨床検査医学会学術集会, 2019年11月. 山口純代, 岩城真帆, 清水郁子, 稲垣太造, 湊将典, 小野広幸, 上田紗代, 西村賢二, 柴田恵理子, 田蒔昌憲, 長井幸二郎, 安部秀斉 :
全身倦怠感，呼吸困難感を生じ，その後急性高Ca血症と判明した透析患者の一例,
第47回徳島透析療法研究会, 2019年11月. 湊将典, 村上太一, 上田紗代, 小野広幸, 西村賢二, 柴田恵理子, 田蒔昌憲, 長井幸二郎, 安部秀斉 :
Fanconi症候群を合併したTubulointerstitial nephritis with IgM-positive plasma cellsの一例,
第49回日本腎臓学会西部学術大会, 2019年10月. 清水郁子, 長井幸二郎, 稲垣太造, 湊将典, 岩城真帆, 山口純代, 上田紗代, 西村賢二, 小野広幸, 柴田恵理子, 田蒔昌憲, 岸史, 村上太一, 岸誠司, 安部秀斉 :
慢性B型肝炎治療中に緩徐に進行する腎機能障害をみとめた一例,
第49回日本腎臓学会西部学術大会, 2019年10月. 近藤広宗, 田蒔昌憲, 湊将典, 稲垣太造, 柴田恵理子, 西村賢二, 小野広幸, 村上太一, 安部秀斉, 長井幸二郎 :
早期診断に基づく分子標的薬治療で救命しえたTAFRO症候群の1例,
第49回日本腎臓学会西部学術大会, 2019年10月. 岸誠司, 小野広幸, 稲垣太造, 湊将典, 西村賢二, 岸史, 上田紗代, 柴田恵理子, 田蒔昌憲, 村上太一, 安部秀斉, 長井幸二郎 :
PR-3 ANCA陽性化膿性脊椎炎合併シャント腎炎の1例,
第49回日本腎臓学会西部学術大会, 2019年10月. 山口純代, 岩城真帆, 清水郁子, 稲垣太造, 湊将典, 小野広幸, 上田紗代, 西村賢二, 柴田恵理子, 田蒔昌憲, 長井幸二郎, 桝田志保, 遠藤逸朗, 安部秀斉 :
透析導入期に急性高Ca血症を生じた一例,
第49回日本腎臓学会西部学術大会, 2019年10月. 岸田盛吾, 田蒔昌憲, 稲垣太造, 湊将典, 岸史, 岸誠司, 村上太一, 安部秀斉, 長井幸二郎 :
血液培養でHelicobacter cinaediを同定した排液培養陰性腹膜透析関連腹膜炎の一例,
第259回徳島医学会学術集会, 2019年8月. 黒澤すみれ, 清水郁子, 稲垣太造, 湊将典, 岩城真帆, 山口純代, 上田紗代, 西村賢二, 小野広幸, 柴田恵理子, 田蒔昌憲, 安部秀斉, 早渕修, 長井幸二郎 :
B型肝炎治療薬によって緩徐に腎機能悪化をみとめた一例,
第259回徳島医学会学術集会, 2019年8月. 西村賢二, 岸誠司, 小野広幸, 岸史, 田蒔昌憲, 村上太一, 安部秀斉, 長井幸二郎 :
生活習慣病リスク増加は腎臓の線維化と老化を加速する,
第62回日本腎臓学会学術総会, 2019年6月. 小野広幸, 安部秀斉, 田蒔昌憲, 冨永辰也, 岸史, 岸誠司, 村上太一, 長井幸二郎, 土井俊夫 :
Smad1とSmad3の新規相互リン酸化制御機構による糖尿病性腎症の病態解析,
第62回日本腎臓学会学術総会, 2019年6月. 西村賢二, 村上太一, 小野広幸, 上田紗代, 柴田恵理子, 田蒔昌憲, 岸誠司, 長井幸二郎, 安部秀斉, 土井俊夫 :
血中HDLアポ蛋白ApoL1はインスリンシグナルに制御され2型糖尿病における糸球体濾過量と相関する,
第62回日本腎臓学会学術総会, 2019年6月. 村上太一, 小野広幸, 島久登, 田代学, 井上朋子, 田蒔昌憲, 川原和彦, 岸誠司, 長井幸二郎, 安部秀斉, 水口潤, 土井俊夫 :
ADPKDにおけるトルバプタン治療反応性と臨床的特徴についての検討,
第62回日本腎臓学会学術総会, 2019年6月. 安部秀斉 :
ミニ腎臓を利用する慢性腎臓病治療のHTPスクリーニングシステム,
メディカルジャパン2019大阪, 2019年2月. 越智ありさ, 櫻井明子, 安部秀斉 :
iPS/ES細胞を用いない，糸球体スフェロイド作成,
第258回徳島医学会学術集会, 2019年2月. 安部秀斉 :
全く新たな，慢性腎臓病・急性腎障害の創薬・診断法樹立のためのミニ腎臓プラットフォーム,
第4回四国オープンイノベーションワークショップin徳島, 2018年12月. 荒瀬美晴, 長井幸二郎, 稲垣太造, 柴田恵理子, 岸史, 田蒔昌憲, 村上太一, 岸誠司, 安部秀斉, 松浦元一 :
尿蛋白減少にシクロスポリンが有効であったアルポート症候群の1例,
日本内科学会第119回四国地方会, 2018年12月. 村上太一, 岸史, 田蒔昌憲, 長井幸二郎, 安部秀斉, 岸誠司, 湊将典, 上田紗代 :
Fanconi症候群を合併したTubulointerstitial nephritis with IgM-positive plasma cellsの一例,
第119回四国地方会, 2018年12月. 緒方良輔, 小林誠司, 角安香里, 松岡瑞季, 村上太一, 稲垣太造, 湊将典, 上田紗代, 小野広幸, 西村賢二, 岸誠司, 安部秀斉, 柴田恵理子, 岸史, 長井幸二郎 :
クリオグロブリン血症性血管炎症例に対してクライオフィルとレーションにて皮膚潰瘍が改善した一例,
第47回徳島透析療法研究会, 2018年11月. 岡田衣世, 田蒔昌憲, 稲垣太造, 湊将典, 岸史, 岸誠司, 村上太一, 長井幸二郎, 安部秀斉, 土井俊夫 :
血液培養でHelicobacter cinaediを同定した廃液培養陰性PD関連腹膜炎の一例,
第24回日本腹膜透析医学会学術集会・総会, 2018年10月. 西村賢二, 田蒔昌憲, 岸史, 村上太一, 岸誠司, 長井幸二郎, 安部秀斉, 土井俊夫 :
適切な腹膜透析廃液培養が早期診断・治療により有用であった真菌性腹膜炎の1例,
第24回日本腹膜透析医学会学術集会・総会, 2018年10月. 田蒔昌憲, 湊将典, 稲垣太造, 村上太一, 岸誠司, 長井幸二郎, 安部秀斉, 土井俊夫 :
腎盂腎炎と鑑別困難であった化膿性脊椎炎に感染後腎炎の合併が疑われた1例,
第48回日本腎臓学会西部学術大会, 2018年9月. 小野広幸, 長井幸二郎, 松浦元一, 稲垣太造, 湊将典, 上田紗代, 西村賢二, 柴田恵理子, 田蒔昌憲, 岸史, 村上太一, 岸誠司, 水口潤, 安部秀斉, 土井俊夫 :
ALK阻害薬関連の進行性腎障害を呈した1例,
第48回日本腎臓学会西部学術大会, 2018年9月. 村上太一, 岸史, 田蒔昌憲, 岸誠司, 長井幸二郎, 安部秀斉 :
多彩な腎病変を合併し細胞表面マーカー染色により肉芽腫性間質性腎炎を診断しえた腎サルコイドーシスの一例,
第48回日本腎臓学会西部学術集会, 2018年9月. 村上太一, 岸史, 田蒔昌憲, 岸誠司, 長井幸二郎, 安部秀斉 :
血栓性微小血管症による急性腎障害で末期腎不全に至ったクリオグロブリン血管炎の一例,
第48回日本腎臓学会西部学術集会, 2018年9月. 宮上慎司, 小野広幸, 岸誠司, 近藤英司, 内藤伸仁, 稲垣太造, 湊将典, 上田紗代, 西村賢二, 柴田恵理子, 田蒔昌憲, 岸史, 村上太一, 安部秀斉, 西岡安彦, 長井幸二郎 :
ANCA関連血管炎との鑑別を要したIgG4関連疾患の1例,
第257回徳島医学会学術集会, 2018年8月. 田蒔昌憲, 冨永辰也, 藤田結衣, 岸史, 岸誠司, 村上太一, 長井幸二郎, 安部秀斉, 土井俊夫 :
レチノイン酸はBmp4遺伝子発現を直接制御して糖尿病マウスの糸球体硬化を改善する,
第61回日本腎臓学会学術総会, 2018年6月. 安部秀斉 :
糖尿病性腎症の進展予防にむけた病期分類- 病理-バイオマーカーを統合した診断法の開発,
AMED 4事業合同成果報告会, 2018年2月. 西村賢二, 岸誠司, 田蒔昌憲, 村上太一, 長井幸二郎, 安部秀斉, 土井俊夫 :
血液透析導入期に発症した左心系感染性心内膜炎の1例,
第48回徳島透析療法研究会, 2017年11月. 湊将典, 岸誠司, 村上太一, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫 :
nivolumabによる治療中にIgA腎症を発症した肺扁平上皮癌の症例,
第47回日本腎臓学会西部学術大会, 2017年10月. 岸誠司, 小幡史明, 田蒔昌憲, 村上太一, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫 :
全身倦怠感と食欲不振をきっかけに診断に至ったNoncrystalline Light Chain Proximal Tubulopathy (LCPT) の一例,
第47回日本腎臓学会西部学術大会, 2017年10月. 村上太一, 安部秀斉, 土井俊夫, 岸誠司, 松浦元一, 長井幸二郎, 三好雅士, 中尾隆之 :
HDLアポ蛋白ApolipoproteinL1の血中濃度の意義についての検討,
第57回日本臨床化学会年次学術集会, 2017年10月. 村上太一, 安部秀斉, 土井俊夫, 岸誠司, 長井幸二郎, 松浦元一, 三好雅士, 中尾隆之, 小谷和彦 :
HDLアポ蛋白ApolipoproteinL1の血中濃度の意義についての検討,
第57回日本臨床化学会年次学術集会, 2017年10月. 小野広幸, 安部秀斉, 上田紗代, 西村賢二, 田蒔昌憲, 村上太一, 岸誠司, 長井幸二郎, 土井俊夫 :
糖尿病性腎症の糸球体硬化抑制過程におけるSmad1の新規リン酸化部位の同定と解析,
第255回徳島医学会学術集会, 2017年8月. 岩城真帆, 湊将典, 岸誠司, 村上太一, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫, 西條敦郎, 西岡安彦 :
ニボルマブの投与を契機としてIgA腎症を発症した扁平上皮癌の1例,
第255回徳島医学会学術集会, 2017年8月. 久保友紀子, 田蒔昌憲, 湊将典, 村上太一, 岸誠司, 長井幸二郎, 安部秀斉, 土井俊夫, 手束文威, 林二三男 :
尿路感染症との鑑別が困難であった化膿性脊椎炎の1例,
第255回徳島医学会学術集会, 2017年8月. 上田紗代, 村上太一, 宮城順子, 稲垣太造, 湊将典, 小野広幸, 小幡史明, 西村賢二, 吉本咲耶, 柴田恵理子, 田蒔昌憲, 岸史, 岸誠司, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫 :
ダクラタスビル・アスナプレビル併用療法およびアジルサルタンで寛解したHCV関連クリオグロブリン腎症の一例,
第255回徳島医学会学術集会, 2017年8月. 西村賢二, 岸誠司, 田蒔昌憲, 村上太一, 長井幸二郎, 安部秀斉, 土井俊夫 :
血液導入期に発症した左心系感染性心内膜炎の1例,
第255回徳島医学会学術集会, 2017年8月. 藤田結衣, 冨永辰也, 櫻井明子, 長井幸二郎, 安部秀斉, 土井俊夫 :
BMP4シグナルが作用するポドサイト障害発生機序の解析,
第255回徳島医学会学術集会, 2017年8月. 稲垣太造, 小野広幸, 岸誠司, 湊将典, 田蒔昌憲, 村上太一, 上田紗代, 柴田恵理子, 岸史, 長井幸二郎, 安部秀斉, 土井俊夫, 松浦元一, 西村賢二, 吉本咲耶 :
脳室ー心房シャント感染に続発したPR3-ANCA陽性シャント感染後腎炎の一例,
第255回徳島医学会学術集会, 2017年8月. 小幡史明, 村上太一, 田蒔昌憲, 岸誠司, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫 :
抗糸球体基底膜抗体値の著明高値を認めた抗糸球体基底膜抗体型腎炎の1例,
第62回日本透析医学会学術集会, 2017年6月. 村上太一, 稲垣太造, 湊将典, 柴田恵理子, 西村賢二, 小野広幸, 上田紗代, 田蒔昌憲, 岸史, 岸誠司, 長井幸二郎, 安部秀斉, 土井俊夫 :
過粘稠症候群に血漿交換が奏功した原発性マクログロブリン血症の一例,
第62回日本透析医学会学術集会, 2017年6月. 小野広幸, 村上太一, 稲垣太造, 上田紗代, 柴田恵理子, 田蒔昌憲, 岸史, 松浦元一, 岸誠司, 長井幸二郎, 安部秀斉, 土井俊夫 :
クリオグロブリン血栓性血管炎に続発した二次性血栓性微少血管症(TMA)に対して血漿交換，血液透析，ステロイド治療で救命しえた一例,
第62回日本透析医学会学術集会, 2017年6月. 上田紗代, 柴田恵理子, 小野広幸, 田蒔昌憲, 村上太一, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫 :
LDL吸着療法とCyAの併用が奏功したネフローゼ症候群の2例,
第62回日本透析医学会学術集会, 2017年6月. 岸誠司, 飛梅亮, 岸潤, 田蒔昌憲, 岸史, 村上太一, 長井幸二郎, 安部秀斉, 土井俊夫 :
くも膜下出血(SAH)とAKIの合併を良好に管理し得たループス腎炎の一例,
日本透析医学会雑誌, 2017年6月. 吉本咲耶, 長井幸二郎, 柴田恵理子, 上田紗代, 小野広幸, 田蒔昌憲, 西村賢二, 岸史, 松浦元一, 岸誠司, 村上太一, 安部秀斉, 土井俊夫 :
慢性腎臓病患者の入院前中後の血清アルブミン濃度と蛋白尿の推移,
第60回日本腎臓学会学術総会, 2017年5月. 田蒔昌憲, 冨永辰也, 藤田結衣, 松浦元一, 岸誠司, 村上太一, 長井幸二郎, 安部秀斉, 土井俊夫 :
レチノイン酸による糖尿病性糸球体硬化分子BMP4制御機構の検討,
第60回日本腎臓学会学術総会, 2017年5月. 村上太一, 岸誠司, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫 :
TGFβトランスジェニックマウスにおけるビタミンD受容体アナログパリカルシトールの腎保護効果,
第60回日本腎臓学会学術総会, 2017年5月. 村上太一, 岸誠司, 長井幸二郎, 松浦元一, 安部秀斉, 土井俊夫, 中尾隆之, 三好雅士 :
HDLアポ蛋白ApolipoproteinL1の血中濃度の意義についての検討,
第13回合同地方会, 2017年2月. 中川裕美, 冨永辰也, 櫻井明子, 藤田結衣, 安部秀斉, 長井幸二郎, 土井俊夫 :
ポドサイトへのBMP4過剰発現による腎組織への影響,
徳島県臨床検査技師会誌第40回徳島県医学検査学会抄録集, 28, 2016年12月. 安部秀斉 :
ミニ腎臓を用いた腎不全・透析への移行を阻止する画期的治療法開発,
第38回バイオ技術シーズ公開会, 2016年12月. 安部秀斉 :
尿が教えてくれた研究の道筋,
第46回日本腎臓学会西部学術大会, 2016年10月. 田蒔昌憲, 安部秀斉, 小野広幸, 上田紗代, 吉本咲耶, 岸史, 松浦元一, 岸誠司, 村上太一, 長井幸二郎, 土井俊夫 :
糞線虫症の関与が疑われた膜性腎症の一例,
第46回日本腎臓学会西部学術大会, 2016年10月. 村上太一, 岸誠司, 土井俊夫, 安部秀斉, 長井幸二郎, 松浦元一 :
ダクラタスビル・アスナプレビル併用療法およびアジルサルタンで寛解したHCV関連クリオグロブリン腎症の一例,
第46回日本腎臓学会西部学術集会, 2016年10月. 岸誠司, 山田諭, 柴田恵理子, 松浦元一, 長井幸二郎, 岸史, 安部秀斉, 土井俊夫 :
初診時に心不全と診断された高齢発症のヒトパルボウイルスB19による急性糸球体腎炎の1例,
日本腎臓学会誌, 2016年10月. 松浦元一, 吉本咲耶, 櫻井明子, 村上太一, 長井幸二郎, 安部秀斉, 土井俊夫 :
DAPIはAL型アミロイド腎症の診断に有用かもしれない,
2016年9月. 松浦元一, 上田紗代, 小野広幸, 吉本咲耶, 柴田恵理子, 田蒔昌憲, 岸史, 岸誠司, 村上太一, 長井幸二郎, 安部秀斉, 土田健司, 水口潤, 土井俊夫 :
DAPIはAL型アミロイド腎症の診断に有用かもしれない,
第59回日本腎臓学会学術総会, 2016年6月. 長井幸二郎, 冨永辰也, 村上太一, 柴田恵理子, 岸誠司, 松浦元一, 安部秀斉, 土井俊夫 :
メサンギウム細胞のin vivoでの機能解析~mTOR経路の活性化は糸球体硬化を誘導する~,
第59回日本腎臓学会学術総会, 2016年6月. 安部秀斉 :
バイオマーカーとしてのexosome,
第59回日本腎臓学会学術総会, 2016年6月. 村上太一, 長井幸二郎, 柴田恵理子, 小野広幸, 上田紗代, 吉本咲耶, 田蒔昌憲, 岸史, 岸誠司, 松浦元一, 安部秀斉, 土井俊夫 :
急性腎不全を呈した原因不明の血栓性微少血管症に血漿交換および副腎皮質ステロイドが奏功した1例,
第61回日本透析医学会学術集会, 2016年6月. 湊将典, 村上太一, 上田紗代, 岸誠司, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫, 近藤真代, 西岡安彦 :
横隔膜交通症の診断および交通部位同定に腹腔シンチグラフィが有用であった1例,
第114回内科四国地方会, 2016年5月. 村上太一, 土井俊夫, 安部秀斉, 松浦元一, 長井幸二郎, 吉本咲耶, 岸誠司, 上田紗代, 小野広幸, 田蒔昌憲 :
徳島大学腎臓内科における多発性嚢胞腎患者の診療現況,
第114回内科学会四国地方会, 2016年5月. 湊将典, 上田紗代, 村上太一, 小野広幸, 吉本咲耶, 柴田恵理子, 田蒔昌憲, 岸史, 岸誠司, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫, 近藤真代, 坂口暁, 西岡安彦, 新井悠太, 新家崇義, 音見暢一, 河北直也, 滝沢宏光, 梶浦耕一郎, 先山正二 :
横隔膜交通症の診断および交通部位同定に腹腔シンチグラフィが有用であった1例,
第252回徳島医学会学術集会, 2016年2月. 細井美希, 松浦元一, 田蒔昌憲, 上田紗代, 小野広幸, 吉本咲耶, 村上太一, 長井幸二郎, 安部秀斉, 土井俊夫 :
微少変化型ネフローゼ症候群を呈し，自然寛解後再発した足細胞陥入糸球体症の1例,
第113回日本内科学会四国地方会, 2015年12月. 田蒔昌憲, 小野広幸, 上田紗代, 吉本咲耶, 柴田恵理子, 松浦元一, 村上太一, 長井幸二郎, 安部秀斉, 土井俊夫 :
腹膜透析によって効率的な自立支援を行えた若年男性の1例,
第21回腹膜透析医学会学術集会・総会, 2015年11月. 櫻井明子, 安部秀斉, 冨永辰也, 三好雅士, 土井俊夫 :
糖尿病のポドサイト障害におけるCXCR7シグナル異常,
中四国支部医学検査学会(第48回), 2015年11月. 松浦元一, 河原加奈, 上田紗代, 小野広幸, 吉本咲耶, 柴田恵理子, 田蒔昌憲, 村上太一, 長井幸二郎, 安部秀斉, 土田健司, 水口潤, 土井俊夫 :
IgA腎症に膜性腎症を合併した2症例,
第45回日本腎臓学会西部学術大会, 2015年10月. 柴田恵理子, 長井幸二郎, 小野広幸, 上田紗代, 吉本咲耶, 田蒔昌憲, 松浦元一, 村上太一, 安部秀斉, 土井俊夫 :
急性腎不全を発症しPEとステロイドで透析離脱できたTMAの一例,
第45回日本腎臓学会西部学術大会, 2015年10月. 小野広幸, 平野隆弘, 櫻井明子, 新井美存, 上田紗代, 柴田恵理子, 吉本咲耶, 田蒔昌憲, 松浦元一, 村上太一, 長井幸二郎, 土井俊夫, 安部秀斉 :
E2A新規結合分子FLASHによるTNFα-p21制御と細胞増殖・老化の調整による腎炎の修復機構,
第6回分子腎臓フォーラム, 2015年9月. 竹内理沙, 野田康裕, 牧野友美, 近田優介, 緒方良輔, 森西啓介, 小林誠司, 柴田恵理子, 長井幸二郎, 村上太一, 松浦元一, 安部秀斉, 土井俊夫, 大西実季, 高松愛子, 山田香苗 :
Pre-pump Arterial Pressureの再評価~実血流と溶血の観点から~,
第60回日本透析医学会学術集会・総会, 2015年6月. 柴田恵理子, 田蒔昌憲, 小野広幸, 上田紗代, 吉本咲耶, 村上太一, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫, 湯浅真由, 久保宜明 :
光線療法に対して難治性でIFN-γを使った菌状息肉症の一例,
第60回日本透析医学会学術集会・総会, 2015年6月. 村上太一, 長井幸二郎, 松浦元一, 田蒔昌憲, 柴田恵理子, 吉本咲耶, 小野広幸, 上田紗代, 安部秀斉, 土井俊夫 :
Trophoblast glycoprotein:ポドサイト障害における発現・機能解析および尿中マーカーとしての検討,
第58回日本腎臓学会学術総会, 2015年6月. 小野広幸, 平野隆弘, 櫻井明子, 新井美存, 上田紗代, 柴田恵理子, 吉本咲耶, 田蒔昌憲, 松浦元一, 村上太一, 長井幸二郎, 土井俊夫, 安部秀斉 :
E2A新規結合因子FLASHによるTNFα-P21制御と細胞増殖・老化の調整による腎炎の修復機構,
第58回日本腎臓学会学術総会, 2015年6月. 村上太一, 長井幸二郎, 松浦元一, 柴田恵理子, 田蒔昌憲, 吉本咲耶, 小野広幸, 上田紗代, 安部秀斉, 土井俊夫 :
Trophoblast glycoprotein:ポドサイト障害における発現・機能解析および尿中マーカーとしての検討,
2015年6月. 安部秀斉 :
尿中エクソソーム・マイクロベジクル,
第58回日本腎臓学会学術総会, 2015年6月. 安部秀斉 :
尿中エクソソーム解析による不可逆的な腎機能低下を予測するバイオマーカーの探索,
腎疾患対策研究事業・難治性疾患等政策研究事業・難治性疾患等実用化研究事業合同研究成果発表会, 2015年2月. 安部秀斉 :
糖尿病患者の血管合併症を判定する尿中バイオマーカー樹立,
2015年2月. 安部秀斉 :
糖尿病患者の血管合併症を判定する尿中バイオマーカー樹立,
Diabetes Masters Conference, 2014年12月. 野田和克, 村上太一, 上田紗代, 柴田理恵子, 田蒔昌憲, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫 :
Dペニシラミン投与後に微小変化型ネフローゼ症候群を発症しミゾリビンが著効した一例,
第111回内科四国地方会, 2014年11月. 櫻井明子, 安部秀斉, 長井幸二郎, 村上太一, 安部尚子, 土井俊夫 :
糖尿病のポドサイト障害におけるBMP-CXCR7シグナル異常の検出法,
第61回日本臨床検査医学会学術集会, 2014年11月. 安部秀斉, 小野広幸, 平野隆弘, 櫻井明子, 土井俊夫 :
FlashとE2Aの新規相互作用はTNF-α-p21によって細胞増殖と細胞老化を制御する,
第37回日本分子生物学会年会, 2014年11月. 吉本咲耶, 長井幸二郎, 小野広幸, 柴田恵理子, 上田紗代, 田蒔昌憲, 安部尚子, 村上太一, 美馬晶, 松浦元一, 安部秀斉, 土井俊夫 :
サルコイドーシス，高カルシウム血症により間質障害を呈した一例,
第44回日本腎臓学会西部学術大会, 2014年10月. 小野広幸, 村上太一, 松浦元一, 美馬晶, 吉本咲耶, 上田紗代, 田蒔昌憲, 柴田恵理子, 長井幸二郎, 安部秀斉, 土井俊夫 :
ループス腎炎との鑑別を要したIgG4関連腎症の1例,
第44回日本腎臓学会西部学術大会, 2014年10月. 松浦元一, 上田紗代, 小野広幸, 吉本咲耶, 柴田恵理子, 田蒔昌憲, 村上太一, 長井幸二郎, 安部秀斉, 佐藤正大, 岸潤, 西岡安彦, 土井俊夫 :
関節リウマチに対してetanercept投与中に半月体形成性糸球体腎炎を来した1例,
第44回日本腎臓学会西部学術大会, 2014年10月. 竹内理沙, 野田康裕, 長井幸二郎, 小野広幸, 吉本咲耶, 牧野友美, 近田優介, 小林誠司, 大西実季, 高松愛子, 山田香苗, 美馬晶, 柴田恵理子, 松浦元一, 安部秀斉, 土井俊夫 :
実血流の確保において引き込みは指標となりうるか,
第59回日本透析医学会学術集会・総会, 2014年6月. 新井悠太, 長井幸二郎, 柴田恵理子, 藤田美香, 美馬晶, 松浦元一, 安部秀斉, 土井俊夫, 宮本龍郎, 土井俊夫 :
抗GBM抗体，P-ANCA陽性急速進行性腎炎の治療経過において視力低下を来した高齢者の一例,
日本内科学会第110回四国地方会, 2014年6月. 安部秀斉 :
生活習慣病とCKD∼治療の選択肢の選び方∼,
第427回徳島県中部臨床研究会, 2013年12月. 櫻井明子, 林早苗, 冨永辰也, 藤田結衣, 安部尚子, 土井俊夫, 安部秀斉 :
糖尿病性腎症におけるmiR-21のポドサイトに対するPDCD4制御を介した抗アポトーシス効果,
第36回日本分子生物学会年会, 2013年12月. 小野広幸, 美馬晶, 吉本咲耶, 松浦元一, 柴田恵理子, 長井幸二郎, 安部秀斉, 土井俊夫 :
H.pylori陽性かつSLEの診断基準を満たす免疫異常に続発したIgG4関連腎症の1例,
日本内科学会第19回四国地方会, 2013年12月. 竹内理沙, 野田康裕, 長井幸二郎, 小野広幸, 吉本咲耶, 牧野友美, 近田優介, 小林誠司, 大西実季, 高松愛子, 山田香苗, 美馬晶, 松浦元一, 柴田恵理子, 安部秀斉, 土井俊夫 :
針の口径によって確保できる実血流量の評価,
第44回徳島透析療法研究会, 2013年11月. 安部秀斉 :
高齢者CKDの降圧治療戦略∼腎機能低下ハイリスク群への対応∼,
高齢者CKDを考える会in徳島, 2013年11月. 小野広幸, 美馬晶, 柴田恵理子, 松浦元一, 山田諭, 長井幸二郎, 吉本咲耶, 安部秀斉, 土井俊夫 :
当院における成人紫斑病性腎炎に対するプレドニゾロン+ミゾリビン併用療法の有効性についての検討,
第43回日本腎臓学会西部学術総会, 2013年10月. 小野広幸, 美馬晶, 柴田恵理子, 松浦元一, 山田諭, 長井幸二郎, 吉本咲耶, 安部秀斉, 土井俊夫, 柴田恵理子 :
当院における成人紫斑病性腎炎に対するプレドニゾロン+ミゾリビン併用療法の有効性についての検討,
第43回日本腎臓学会西部学術総会, 2013年10月. 安部秀斉 :
慢性腎臓病CKDの最近の診断と治療,
南あわじ市医師会臨床談話会, 2013年9月. Fujita Yui, Akiko Sakurai, Tatsuya Tominaga, Hayashi Sanae, Naoko Abe, Toshio Doi and Hideharu Abe :
Multiple regulatory pathways of BMP-Smad axis through a sclerosis-specific basic HLH transcription factor in diabetic nephropathy.,
第86回日本生化学会大会, Sep. 2013. 安部尚子, 安部秀斉, 土井俊夫, Hayashi Sanae :
腎機能低下予測バイオマーカーとしてのポドサイト由来エクソソーム内転写因子,
第53回日本臨床化学会年次学術集会, 2013年9月. 安部秀斉 :
腎臓をよく診ると血糖管理法が見えてくる,
心・腎からみた血管合併症治療戦略in徳島, 2013年7月. 野田康裕, 竹内理沙, 長井幸二郎, 久原幸典, 近田優介, 小林誠司, 山田香苗, 高松愛子, 美馬晶, 松浦元一, 三並智子, 柴田恵理子, 安部秀斉, 土井俊夫 :
針の口径による最大血流量と TR-3000測定血液流量モニタリングシステムの評価,
第58回日本透析医学会学術集会・総会, 2013年6月. 安部秀斉 :
糖尿病とCKDの実情,
第41回徳島循環器フォーラム, 2013年6月. 三好雅士, 長井幸二郎, 掛武威, 福島直, 松浦元一, 柴田恵理子, 吉川和寛, 山口邦久, 井崎博文, 美馬晶, 冨永辰也, 安部秀斉, 土井俊夫 :
ヒトIgA腎症におけるGas6とその受容体Dtkの関与,
第56回日本腎臓学会学術総会, 2013年5月. 安部秀斉 :
糖尿病性腎症における硬化促進転写因子の解析,
第5回四国ネフロロジー研究会, 2013年3月. 安部秀斉 :
糖尿病性腎症:臨床上の問題点への分子病態からのアプローチ,
第15回徳島総合診療研究会, 2013年2月. 安部秀斉 :
生活習慣病とCKD,
徳島高血圧治療学術講演会, 2013年2月. 安部秀斉 :
高齢者CKDの降圧療法,
ARB Forum 2012, 2013年1月. 安部秀斉 :
糸球体腎炎におけるCD44作用機序の解析,
第85回日本生化学会大会, 2012年12月. 安部秀斉 :
BMP4シグナル活性化はポドサイト障害およびメサンギウム基質増生を進展させる,
第85回日本生化学会大会, 2012年12月. Naoko Abe and Hideharu Abe :
Predictive biomarkers for kidney function declines: podocyte-derived exosomal transcriptional factors,
第35回日本分子生物学会年会, Dec. 2012. 古本哲朗, 安部秀斉 :
17歳で巣状糸球体硬化症を呈した低出生体重児の1例,
第107回日本内科学会四国地方会, 2012年12月. 古本哲朗, 長井幸二郎, 山田諭, 柴田恵理子, 岸史, 岸誠司, 松浦元一, 美馬晶, 安部秀斉, 土井俊夫, 竹内理沙, 野田康裕, 小林誠司, 近田優介, 高松愛子, 山田香苗, 長江雄浩, 中瀧理仁 :
血液透析によってリチウム中毒による意識障害の改善をみた1症例,
第43回徳島透析療法研究会, 2012年11月. 安部秀斉 :
糖尿病とCKDの本当の関係,
鳥取県西部トラゼンタ錠発売1周年記念講演会, 2012年11月. 安部秀斉 :
CKD∼診療の実際と問題点∼,
那賀町CKDカンファレンス, 2012年11月. 松浦元一, 山田諭, 柴田恵理子, 渡瀬謙仁, 岸史, 岸誠司, 美馬晶, 長井幸二郎, 安部秀斉, 中村信元, 安倍正博, 土井俊夫 :
腎生検にてγ重鎖沈着症が疑われた糸球体沈着症の一例,
第42回日本腎臓学会西部学術大会, 2012年10月. 冨永辰也, 安部秀斉, 長井幸二郎, 岸誠司, 美馬晶, 土井俊夫 :
BMP4シグナル活性化はポドサイト障害およびメサンギウム基質増生を進展させる,
第3回分子腎臓フォーラム, 2012年9月. 安部秀斉 :
CKD患者の貧血と治療,
小松島市医師会学術講演会, 2012年7月. 安部秀斉 :
CKDの診方・考え方,
第3回徳島メディカルサークル, 2012年7月. 安部秀斉 :
CKD診療の実際∼一般内科から専門医に患者を紹介するタイミング∼,
ステップアップセミナー, 2012年7月. 安部秀斉 :
糖尿病患者のCKD治療とCKD患者の糖尿病治療,
第2回慢性腎臓病を考える会in愛媛, 2012年7月. 冨永辰也, 安部秀斉, 長井幸二郎, 岸誠司, 美馬晶, 土井俊夫 :
糖尿病性腎症におけるポドサイト障害に作用するBMP4の分子機構,
第4回腎疾患と高血圧研究会, 2012年7月. 安部尚子, 安部秀斉 :
糖尿病合併透析患者でのアログリプチンの長期的有効性,
第57回日本透析医学会学術集会・総会, 2012年6月. 柴田恵理子, 長井幸二郎, 山田諭, 渡瀬謙仁, 岸史, 岸誠司, 松浦元一, 安部秀斉, 土井俊夫 :
中等度以上腎機能低下患者に対するフェブキソスタットの有効性の検討,
第55回日本腎臓学会学術総会, 2012年6月. 三好雅士, 長井幸二郎, 掛武威, 福島直, 松浦元一, 柴田恵理子, 山田諭, 渡瀬謙仁, 吉川和寛, 岸史, 岸誠司, 山口邦久, 井崎博文, 冨永辰也, 安部秀斉, 土井俊夫 :
ヒトIgA腎症における増殖因子Gas6とその受容体Axlの発現,
第55回日本腎臓学会学術総会, 2012年6月. 冨永辰也, 安部秀斉, 長井幸二郎, 岸誠司, 土井俊夫 :
ポドサイト障害におけるアポトーシス誘導メカニズムに関する新しい知見,
第4回四国ネフロロジー研究会, 2012年3月. 安部秀斉 :
CKDの真の姿をどうとらえるか∼腎臓内科外来診療の実際∼,
脂質異常症とCKDを考える会, 2012年2月. 安部秀斉 :
糖尿病性腎症の分子病態と新規診断・治療,
第59回香川腎疾患談話会, 2012年2月. 安部秀斉 :
CKDの診かた,
第170回名西郡医師会学術講演会, 2012年2月. 安部秀斉 :
慢性腎臓病患者の診断と治療のための新規尿中バイオマーカー,
第12回大学発・選り抜きバイオセミナー, 2011年12月. 山田諭, 長井幸二郎, 中村雅将, 柴田恵理子, 松浦元一, 村上太一, 荒岡利和, 岸誠司, 安部秀斉, 土井俊夫 :
透析導入により痙攣，意識障害，消化器症状の改善が見られた1例,
第42会徳島透析療法研究会, 2011年11月. 安部秀斉, 林早苗 :
尿中エクソゾームを用いた慢性腎臓病の非侵襲的診断法と予後予測,
日本分子生物学会年会, 2011年11月. 林早苗, 安部秀斉 :
尿中エクソゾームを用いた慢性腎臓病の非侵襲的診断法と予後予測,
第34回日本分子生物学会年会, 2011年11月. 山田諭, 岸誠司, 柴田恵理子, 松浦元一, 長井幸二郎, 安部秀斉, 土井俊夫, 小笠原梢, 佐田政隆 :
ヒトパルボウィルスB19による急性糸球体腎炎の1例,
第105回日本内科学会四国地方会, 2011年11月. 安部秀斉 :
糖尿病と腎障害,
徳島HEART RENAL JOINT FORUM, 2011年10月. 安部秀斉 :
糖尿病性腎症の分子病態と分子標的治療,
第5回代謝異常とCKDを考える会学術講演会, 2011年10月. 安部秀斉 :
糖尿病性腎症の分子病態―BMP4-Smad1シグナル,
第41回日本腎臓学会西部学術総会, 2011年9月. 山田諭, 長井幸二郎, 上田恵理子, 村上太一, 松浦元一, 岸誠司, 安部秀斉, 土井俊夫, 遠藤逸郎, 松本俊夫 :
活性型ビタミンD3外用剤による高カルシウム血症由来の腎機能障害の一例,
日本腎臓学会雑誌, Vol.53, No.6, 815, 2011年8月. 柴田恵理子, 長井幸二郎, 村上太一, 山田諭, 岸誠司, 松浦元一, 安部秀斉, 土井俊夫, 板東良美, 津田恵, 高橋正幸, 金山博臣 :
腎細胞癌に対する受容体チロシンキナーゼ阻害薬Sunitinib投与にてThrombotic microangiopathyを来した一例,
日本腎臓学会雑誌, Vol.53, No.6, 794, 2011年8月. 安部秀斉 :
CKD:ホントのところ -診療の実際-,
第15回診療のツボ勉強会, 2011年6月. 吉川和寛, 安部秀斉, 松浦元一, 長井幸二郎, 土井俊夫 :
Genomic biomarkerを用いたCKD患者の心血管リスク評価の試み,
第56回日本透析医学会学術集会・総会, 2011年6月. 山下陽子, 浜田優介, 高木優, 山田香苗, 高松愛子, 上田雅彦, 山口邦久, 金山博臣, 近藤直樹, 岸史, 岸誠司, 荒岡利和, 松浦元一, 村上太一, 安部秀斉, 中村雅将, 長井幸二郎, 土井俊夫 :
糖尿病合併血液透析患者の自然分娩に至った1例,
日本透析医学会学術集会, 2011年6月. 松原雄, 安部秀斉 :
糖尿病性腎症における糸球体硬化とアルブミン尿には異なる病態形成機構が存在する,
第54回日本腎臓学会学術総会, 2011年6月. 冨永辰也, 安部秀斉 :
BMP4における糖尿病性腎症の発症とアルブミン尿排泄に関する新たな機序,
第54回日本糖尿病学会年次学術集会, 2011年5月. 石澤有紀, 村上太一, 岸史, 松浦元一, 近藤直樹, 岸誠司, 長井幸二郎, 安部秀斉, 土井俊夫 :
LDL吸着が複数回奏功した難治性ネフローゼ症候群の1例,
日本内科学会第104会四国地方会, 2011年5月. 冨永辰也, 安部秀斉, 長井幸二郎, 岸誠司, 土井俊夫 :
糖尿病性腎症発症とアルブミン尿排泄に関与するBMP4の分子機構,
第52回日本生化学会中国・四国支部例会, 2011年5月. 松原雄, 安部秀斉, 上田乙也, 寺社下浩一, 美馬晶, 後藤千里, 荒木真, 鳥越和雄, 長井幸二郎, 家原典之, 福島直, 深津敦司, 木野崎雅彦, 荒井秀典, 土井俊夫 :
糖尿病性腎症における糸球体硬化とアルブミン尿には異なる病態形成機構が存在する,
日本腎臓学会誌, Vol.53, No.3, 390, 2011年5月. 冨永辰也, 安部秀斉, 村上太一, 岸誠司, 長井幸二郎, 土井俊夫 :
BMP4における糖尿病性腎症の発症とアルブミン尿排泄機序に関する新たな機序,
糖尿病, Vol.54, No.Suppl.1, S-326, 2011年4月. 安部秀斉 :
慢性腎臓病患者の診断・治療のための新規バイオマーカー,
第10回次世代医療システム産業化フォーラム2010, 2011年3月. 冨永辰也, 安部秀斉 :
腎発生に必須なBMP4が関与する糖尿病性腎症発症の分子機構,
第83回日本生化学会大会, 2010年12月. 冨永辰也, 安部秀斉 :
腎発生に必須なBMP4が関与する糖尿病性腎症発症の分子機構,
第33回日本分子生物学会年会, 2010年12月. 安部尚子, 安部秀斉, 近藤直樹, 吉川和寛, 土井俊夫 :
新規バイオマーカーとしてのpodocyte由来尿中エクソゾームによる慢性腎臓病患者の病態解析,
第83回日本生化学会大会, 2010年12月. 安部尚子, 安部秀斉, 近藤直樹, 吉川和寛, 土井俊夫 :
新規バイオマーカーとしてのpodocyte由来尿中エクソゾームによる慢性腎臓病患者の病態解析,
第33回日本分子生物学会年会, 2010年12月. 安部秀斉 :
糖尿病性腎症の新たなターゲットと治療戦略,
第31回日本臨床薬理学会年会, 2010年12月. 崎山勉, 村上太一, 安部秀斉 :
早期治療が奏功したGoodpasture症候群の1例,
第103回日本内科学会四国地方会, 2010年11月. 長井幸二郎, 岸史, 岸誠司, 中村雅将, 村上太一, 松浦元一, 荒岡利和, 近藤直樹, 美馬晶, 安部秀斉, 土井俊夫 :
多彩な合併症のある高齢者コレステロール塞栓の2例,
第40回日本腎臓学会西部学術大会, 2010年10月. 荒岡利和, 安部秀斉, 長井幸二郎, 松浦元一, 村上太一 :
ミゾリビン500mg投与が有効であった，ステロイド及びシクロスポリンA治療抵抗性成人膜性腎症の一例,
第40回日本腎臓学会西部学術大会, 2010年10月. 安部秀斉 :
糖尿病性腎症の病因解析の進歩,
第21回日本臨床化学会東海・北陸支部総会シンポジウム, 2010年8月. 荒岡利和, 安部秀斉, 長井幸二郎, 松浦元一, 村上太一, 岸誠司, 岸史, 近藤直樹, 土井俊夫 :
ミゾリビン500mg投与が有効であった，ステロイド及びシクロスポリンA治療抵抗性成人膜性腎症の一例,
日本腎臓学会, Vol.52, No.6, 828, 2010年8月. 長井幸二郎, 岸史, 岸誠司, 中村雅将, 村上太一, 松浦元一, 荒岡利和, 近藤直樹, 美馬晶, 安部秀斉, 土井俊夫 :
多彩な合併症のある高齢者コレステロール塞栓の2例,
日本腎臓学会誌, Vol.52, No.6, 803, 2010年8月. 荒岡利和, 安部秀斉, 長井幸二郎, 松浦元一, 村上太一, 岸誠司, 岸史, 近藤直樹, 土井俊夫 :
ミゾリビン500mg投与が有効であった，ステロイド及びシクロスポリンA治療抵抗性成人膜性腎症の一例,
日本腎臓学会誌, Vol.52, No.6, 828, 2010年8月. 舩瀬公博, 安部尚子, 安部秀斉 :
東レ・メディカル社製透析管理システムと電子カルテ連携による効率化,
第55回日本透析医学会学術集会・総会, 2010年6月. 吉川和寛, 安部秀斉, 冨永辰也 :
CKD患者の血中MGPおよび関連分子と，病態に関する検討,
第55回日本透析医学会学術集会・総会, 2010年6月. 近藤直樹, 安部秀斉 :
新規バイオマーカーとしての尿中エクソゾーム中のCD2APによるCKD患者の予後解析,
第55回日本透析医学会学術集会・総会, 2010年6月. 安部秀斉, 土井俊夫 :
糖尿病性腎症の分子病態―BMP4-Smad1の役割,
第53回日本腎臓学会学術総会シンポジウム, 2010年6月. 松原雄, 安部秀斉, 上田乙也 :
糖尿病性腎症に関わる新たな治療標的分子の検討,
第53回日本腎臓学会学術総会, 2010年6月. 岸誠司, 安部秀斉, 岸史, 吉川和寛 :
メサンギウム細胞(MCs)の軟骨細胞形質獲得と低酸素下での不可逆的な腎機能低下の関連,
第53回日本腎臓学会学術総会, 2010年6月. 高松典通, 安部秀斉, 冨永辰也, 長井幸二郎, 土井俊夫 :
地域住民健診におけるアルブミン尿検出の有用性,
第53回日本腎臓学会学術総会, 2010年6月. 岸誠司, 安部秀斉, 岸史, 吉川和寛, 荒岡利和, 村上太一, 冨永辰也, 長井幸二郎, 美馬晶, 家原典之, 秋山治彦, 土井俊夫 :
メサンギウム細胞(MCs)の軟骨細胞形質獲得と低酸素下での不可逆的な腎機能低下の関連,
日本腎臓学会誌, Vol.52, No.3, 322, 2010年5月. 近藤直樹, 安部秀斉, 芦名茂人, 吉川和寛, 岸史, 荒岡利和, 岸誠司, 松浦元一, 富永辰也, 村上太一, 中村雅将, 長井幸二郎, 土井俊夫 :
新規バイオマーカーとしての尿中エクソゾーム中のCD2APによるCKD患者の予後解析,
日本透析医学会雑誌, Vol.43, No.Suppl.1, 801, 2010年5月. 松原雄, 安部秀斉, 上田乙也, 寺社下浩一, 美馬晶, 後藤千里, 冨永辰也, 荒木真, 鳥越和雄, 長井幸二郎, 家原典之, 福島直, 木野崎雅彦, 深津敦司, 荒井秀典, 土井俊夫 :
糖尿病性腎症に関わる新たな治療標的分子の検討,
日本腎臓学会誌, Vol.52, No.3, 288, 2010年5月. 高松典通, 安部秀斉, 冨永辰也, 長井幸二郎, 土井俊夫 :
地域住民健診におけるアルブミン尿検出の有用性,
日本腎臓学会誌, Vol.52, No.3, 299, 2010年5月. 吉川和寛, 安部秀斉, 冨永辰也, 岸誠司, 岸史, 荒岡利和, 村上太一, 近藤直樹, 松浦元一, 長井幸二郎, 土井俊夫, 中村雅将, 土田健司, 水口潤, 川島周 :
CKD患者の血中MGPおよび関連分子と，病態に関する検討,
日本透析医学会雑誌, Vol.43, No.Suppl.1, 682, 2010年5月. 冨永辰也, 安部秀斉, 長井幸二郎, 美馬晶, 村上太一, 荒岡利和, 岸誠司, 繁田令子, 土井俊夫 :
糖尿病性腎症の発症・進展にBMP4/Smad1経路が重要な作用をおよぼす,
日本臨床分子医学会学術総会プログラム・抄録集, 66, 2010年4月. 松原雄, 安部秀斉, 上田乙也, 寺社下浩一, 美馬晶, 長井幸二郎, 松浦元一, 家原典之, 深津敦司, 荒井秀典, 土井俊夫 :
Smad1は糖尿病性糸球体硬化症の進展に重要な役割を果たす,
日本臨床分子医学会学術総会プログラム・抄録集, 67, 2010年4月. 岸誠司, 安部秀斉, 岸史, 荒岡利和, 村上太一 :
Chondrogenic potential of mesangial cells in diabetic nephropathy,
第2回四国ネフロロジー研究会, 2010年3月. 芦名茂人, 安部秀斉, 土井俊夫 :
加齢による影響を受けない腎症新規バイオマーカーの探索,
第21回日本老年医学会四国地方会総会, 2010年2月. 平野隆弘, 安部秀斉, 奥本陽子 :
Flashはメサンギウム細胞においてE2AおよびP21WAF1/CIP1を介し細胞増殖および細胞老化を制御する,
第21回日本老年医学会四国地方会総会, 2010年2月. 高松典通, 安部秀斉, 冨永辰也, 奥本陽子 :
65歳以上の腎機能低下関連因子--横断的研究による検討,
第21回日本老年医学会四国地方会総会, 2010年2月. 安部秀斉 :
CKDの実際∼治療の考え方∼,
阿南市医師会学術会講演会, 2010年2月. 村上太一, 安部秀斉, 冨永辰也, 荒岡利和, 岸誠司, 高松典通, 美馬晶, 長井幸二郎, 高井義美, 土井俊夫 :
糸球体上皮細胞のアクチン骨格制御におけるTrophoblast glycoproteinの機能,
日本生化学会大会プログラム・講演要旨集, 2P-697, 2009年10月. 荒岡利和, 安部秀斉, 松浦元一, 村上太一, 岸誠司, 岸史, 吉川和寛, 繁田令子, 長井幸二郎, 冨永辰也, 土井俊夫 :
2型糖尿病原因遺伝子TCF7L2を介した糖尿病性腎症感受性遺伝子ALK1の分子調節機構の解析,
日本生化学会大会プログラム・講演要旨集, 4T10a-18, 2009年9月. 冨永辰也, 安部秀斉, 長井幸二郎, 美馬晶, 村上太一, 荒岡利和, 岸誠司, 繁田令子, 上田乙也, 後藤千里, 寺社下浩一, 木野崎雅彦, 福島直, 土井俊夫 :
糖尿病性腎症の発症・進展にBMP4/Smad1経路が重要な作用をおよぼす,
日本生化学会大会プログラム・講演要旨集, 4T10a-14, 2009年9月.

研究会・報告書: 稲垣太造, 長井幸二郎, 岸史, 柴田恵理子, 菊池高史, 湊将典, 小幡史明, 西村賢二, 小野広幸, 上田紗代, 竹内理沙, 緒方良輔, 小林誠司, 松岡瑞季, 角安香里, 高松愛子, 山田香苗, 向井香奈子, 河内綾香, 宮本悠香, 吉本咲耶, 松浦元一, 田蒔昌憲, 村上太一, 岸誠司, 安部秀斉, 土井俊夫 :
ANCA関連腎炎に腹部大動脈瘤を合併し対応に苦慮した一例,
第47回徳島透析療法研究会, 2016年11月. 村上太一, 長井幸二郎, 松浦元一, 安部秀斉, 土井俊夫 :
血液透析患者の貧血治療における鉄補充方法の検討:クエン酸第一鉄経口投与の評価,
第49回四国透析療法研究会, 2015年10月. 冨永辰也, 安部秀斉, 長井幸二郎, 美馬晶, 村上太一 :
腎発生に必須なBMP4が関与する糖尿病性腎症発症の分子機構,
第3回四国ネフロロジー研究会, 2011年3月. 安部秀斉 :
微量アルブミン尿,
糖尿病とCKD講演会, 2011年1月. 安部秀斉 :
CKD∼ESRDの診断と治療,
阿波・吉野川市地域医療勉強会, 2010年12月. 安部秀斉 :
腎機能低下糖尿病患者の治療,
徳島県ジャヌビアSpeakersForum, 2010年12月. 近藤直樹, 岸史, 岸誠司, 松浦元一, 村上太一, 長井幸二郎, 安部秀斉 :
自然分娩に至ったⅠ型糖尿病合併透析患者の1 例,
第41 回徳島透析療法研究会, 2010年11月. 安部秀斉 :
糖尿病性腎症における糸球体硬化を反映するバイオマーカーの樹立,
The 4th Diabetes Masters Conference 学術講演会, 2010年11月. 安部秀斉 :
糖尿病性腎症のUp to date,
第41回静岡腎セミナー, 2010年9月. 安部秀斉 :
実地医家における高血圧治療の現状と最適な薬剤選択について,
徳島総合診療研究会, 2010年9月. 安部秀斉 :
CKDの降圧療法,
『腎臓』に関する勉強会, 2010年8月. 安部秀斉, 冨永辰也, 土井俊夫 :
BMP4活性化によるアルブミン尿出現の新規メカニズムの解明,
第2回腎疾患と高血圧研究会, 2010年7月. 安部秀斉 :
CKDの実際∼糖尿病性腎症を中心に∼,
第383回徳島県中部臨床研究会, 2010年4月. 安部秀斉 :
ESRDの見方について,
吉野川市Small Meeting, 2010年4月. 安部秀斉 :
CKDの実際∼治療の考え方∼,
阿波病院臨床研究会, 2010年2月. 美馬晶, 荒井秀典, 松原雄, 金森弘志, 角栄里子, 家原典之, 深津敦司, 安部秀斉, 高橋利和, 冨永辰也, 北徹, 土井俊夫 :
アンギオテンシンII受容体拮抗薬は糖尿病性腎症においてSrc/Smad1系を抑制することにより糸球体硬化を抑制する,
シンポジウム糖尿病, 2005年10月. 美馬晶, 松原雄, 長井幸二郎, 金森弘志, 角栄里子, 家原典之, 深津敦司, 荒井秀典, 安部秀斉, 土井俊夫 :
アンギオテンシンII受容体拮抗薬は糖尿病性腎症における糸球体硬化に関わるSrc/Smad1系を抑制する,
第11回分子腎臓研究会, 2005年10月.

特許: 安部秀斉, 右手浩一 : 粒子を分級するための高吸水性ポリマー，及びそれを用いた分級方法, 特願2020-102227 (2020年6月), 特許第03262020JP号 (2020年6月). 安部秀斉 : 腎臓疾患に関するマーカー及びその利用, (2015年3月), 特許第PCT/JP2015/056232号 (2015年3月). 安部秀斉 : 慢性腎臓病の腎機能低下予測，及びその治療効果判定方法, (2014年3月), 特許第2014-041531号 (2014年3月). 安部秀斉 : 糖尿病性腎症の検出方法及びキット，糖尿病性腎症の予防及び/又は治療剤，ならびに糖尿病性腎症の予防及び/又は治療に有効な物質を同定する方法及びキット, (2003年9月), 特許第PCT/JP2004/13124号 (2003年9月).
作品: 研究者総覧に該当データはありませんでした。
補助金・競争的資金: DKDが近年増加している原因の分子メカニズムの解明 (研究課題/領域番号: 20K08593 )
糖尿病における進行性腎障害の病態特異的バイオマーカー樹立と修復機構解明 (研究課題/領域番号: 18K08245 )
糖尿病性腎症における特異的ポドサイト障害分子の同定と尿中バイオマーカーの樹立 (研究課題/領域番号: 18K07415 )
サイトカインプロセシング酵素を標的にした新規CKD治療薬の開発 (研究課題/領域番号: 17K09700 )
糖尿病性腎症および腎硬化症の血管合併症分子病態解明とその修復法の開発 (研究課題/領域番号: 15K09265 )
加齢に伴うネフロン減少の分子病態の解明 (研究課題/領域番号: 24591201 )
尿中エクソゾーム解析による非侵襲的腎臓病診断法の確立 (研究課題/領域番号: 23659445 )
RA系非依存的な糖尿病性腎症の発症予測バイオマーカーと分子標的治療法の開発 (研究課題/領域番号: 22390169 )
加齢と腎障害を架橋する新規シグナル伝達経路の解明 (研究課題/領域番号: 21790808 )
慢性腎臓病から腎不全に至る不可逆的形質変化の分子機構解明 (研究課題/領域番号: 21591033 )
加齢性腎障害における新たな分子機構の解明 (研究課題/領域番号: 19790580 )
BMP/ALK/Smad1の解析による糸球体硬化症機構解明とバイオマーカーの同定 (研究課題/領域番号: 19590973 )
腎特異的な形質変換規定因子のクローニングと機能解析 (研究課題/領域番号: 17659257 )
糖尿病性腎症進展制御分子Smadlの関連分子群の解析による腎症発症機構の解明 (研究課題/領域番号: 17590853 )
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2023年3月22日更新

専門分野・研究分野: 腎臓学 (Nephrology)
所属学会・所属協会: 日本内科学会
日本腎臓学会
日本透析医学会
日本老年医学会
委員歴・役員歴: 日本内科学会 (専門医 [2001年12月〜2017年12月], 認定医 [1997年4月〜2017年12月], 指導医 [2008年4月〜2016年3月], 四国支部評議員 [2008年4月〜2016年3月])
日本腎臓学会 (専門医 [2009年4月〜2018年12月])
日本透析医学会 (専門医 [2010年4月〜2018年12月])
日本老年医学会 (評議員 [2011年4月〜2018年12月])
受賞: 2010年7月, 研究賞 (腎疾患と高血圧研究会)
2012年8月, 近藤記念医学財団学術奨励賞 (近藤記念医学財団)
活動: 外来医長 (2008年4月〜2015年3月)
准教授 (2009年7月〜2015年3月)
副科長 (2009年7月〜2015年3月)

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2023年3月19日更新

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Ｊグローバル

Jグローバル最終確認日: 2023/3/18 01:18
氏名（漢字）: 安部秀斉
氏名（フリガナ）: アベヒデハル
氏名（英字）: Abe Hideharu
所属機関: 徳島大学大学院准教授

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researchmap最終確認日: 2023/3/19 01:16
氏名（漢字）: 安部秀斉
氏名（フリガナ）: アベヒデハル
氏名（英字）: Abe Hideharu
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登録日時: 2008/11/14 00:00
更新日時: 2018/11/8 20:05
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所属ID: 0344000000
所属: 徳島大学大学院
部署: 腎臓内科学
職名: 准教授
学位: 医学博士
学位授与機関: 京都大学大学院
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研究者番号: 60399342

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所属（過去の研究課題 情報に基づく）*注記: 2018/4/1 – 2021/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 准教授
2016/4/1 – 2017/4/1 : 徳島大学, 大学院医歯薬学研究部(医学系), 准教授
2015/4/1 : 徳島大学, 大学院医歯薬学研究部, 准教授
2011/4/1 – 2014/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 准教授
2012/4/1 : 徳島大学, 大学院・へルスバイオサイエンス研究部, 准教授
2009/4/1 – 2012/4/1 : 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 准教授
2008/4/1 : 徳島大学, 医学部・歯学部附属病院, 講師
2007/4/1 : 生産開発科学研究所, 腎病態解析研究室, 研究員
2005/4/1 – 2006/4/1 : (財)生産開発科学研究所, 腎病態解析研究室, 研究員
2005/4/1 – 2006/4/1 : 財団法人生産開発科学研究所, 腎病態解析研究室, 研究員

審査区分/研究分野

研究代表者

生物系 / 医歯薬学 / 内科系臨床医学 / 腎臓内科学
小区分53040:腎臓内科学関連

研究代表者以外

生物系 / 医歯薬学 / 内科系臨床医学 / 腎臓内科学
小区分52010:内科学一般関連
小区分53040:腎臓内科学関連

キーワード

研究代表者

腎臓学 / 糖尿病性腎症 / コラーゲン / BMPs / Smad1 / ALK1 / バイオマーカー / 分子病態 / メサンギウム細胞 / Sox9 / BMP4 / 軟骨細胞様形質変化 / 不可逆的腎機能低下 / ALK3/6 / Scleraxis / HIF1 / ALK3 / 6 / 慢性腎臓病 / 細胞老化 / 加齢 / ネフロン / CKD / 腎機能低下 / ネフロン数 / 糖尿病 / BMP / SMA / AGE / smad1 / Id2 / ALK / diabetic nephropathy / α-smooth muscle actin / angiotensin II / type IV collagen / glomerulosclerosis / Src / 腎硬化症 / 腎臓病修復学 / 糸球体硬化 / 細動脈硬化 / 糸球体用スフェロイド / exosome / Liquid Biopsy / 糸球体様スフェロイド / 早期老化 / nephroid / 修復

研究代表者以外

メサンギウム細胞 / 形質変換 / bHLH型転写因子 / Id2 / smooth muscle αactin / 腎臓病理 / 糸球体硬化 / 老化 / 細胞・組織 / 病理学 / BMP4 / 糖尿病性腎症 / Smad1 / Sox9 / バイオマーカー / 抗体医療 / BMP / ALK3/6 / 分子標的治療 / 慢性腎臓病 / エクソゾーム / CKD / ポドサイト / エクソソーム / ALK1 / サイトカイン / PACE4 / 糖尿病 / ポドサイト障害 / 腎硬化症 / Estrogen / 糖尿病性腎臓病(DKD) / 動脈硬化 / 高血圧 / ERR

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