Analysis of Molecular Mechanisms of Podocyte Injury and Its Prevention
| Project/Area Number |
21591019
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Gunma University |
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Principal Investigator |
HIROMURA Keiju 群馬大学, 大学院・医学系研究科, 准教授 (70292597)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 足細胞 / ネフローゼ症候群 / 蛋白尿 / 細胞内シグナル伝達経路 / DNAメチル化 / 内科 / 腎臓内科 / シグナル伝達 / 糸球体 / 糸球体上皮細胞 / SIRP-α / 糖尿病性腎症 / 糖尿病 |
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| Research Abstract |
We have examined the molecular mechanisms of podocyte injury and found the 3 following results. 1) Mizoribine directly inhibits puromycin aminonucleoside-induced podocyte injury through the mechanism independent from IMPDH inhibition. 2) The mice that express mutant SIRP. lacking cytoplasmic region show flatted and irregularly arranged foot processes. In addition, the mutant mice are sensitive to diabetic nephropathy, suggesting that SIRP. and its downstream signalling pathway are involved in the progression of diabetic nephropathy. 3) TGF-β1 induces DNA methylation of WT1 promoter in cultured podocytes. However, the degree of DNA methylation was modest, suggesting that the possibility of methylation of the upstream region of that we have examined or methylation of the promoter of WT1-related molecules.
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Report
(4 results)
Research Products
(24 results)
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[Journal Article] Dendritic Cell-Specific Ablation of the Protein Tyrosine Phosphatase Shpl Promotes Th1 Cell Differentiation and Induces Autoimmunity2012
Author(s)
Kaneko T, Saito Y, Kotani T, Okazawa H, Iwamura H, Sato-Hashimoto M, Kanazawa Y, Takahashi S, Hiromura K, Kusakari S, Kaneko Y, Murata Y, Ohnishi H, Nojima Y, Takagishi K, Matozaki T
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Journal Title
Related Report
Peer Reviewed
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