Molecular mechanisms of promotion or suppression in renal tubular interstitial fibrosis
Project/Area Number |
21590444
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Experimental pathology
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Research Institution | Wakayama Medical University |
Principal Investigator |
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Project Period (FY) |
2009 – 2011
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Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 疾患モデル動物 / 線維化 / 上皮間葉転換 / TGF-β / 腎尿細管 / TGF-βシグナル / EMT / TRPS1 / Smad3 / 腎 / Trps1 / Arkadia / Smad7 / Trpsl |
Research Abstract |
Mutations in TRPS1 cause tricho-rhino-pharyngeal syndrome. Trps1 is essential for nephron development, acting downstream of Bmp7. Because Bmp7 counteracts epithelial-to-mesenchymal transition(EMT) and reverses chronic renal injury, we examined the function of Trps1 in renal fibrosis. The results of the experiment suggest that Trps1 deficiency enhances TGF-b1-induced EMT and tubulointestinal fibrosis by modulating the amount of Smad7 through Arkadia/ubiquitin-mediated degradation.
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Report
(4 results)
Research Products
(31 results)
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[Journal Article] Tolvaptan, a selective oral vasopressin V2 receptor antagonist, ameliorates podocyte injury in puromycin aminonucleoside nephrotic rats2009
Author(s)
Okada T, Sakaguchi T, Hatamura I, Saji F, Negi S, Otani H, Muragaki Y, Kawachi H, Shigematsu T.
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Journal Title
Clinical Experimental Nephrology 13
Pages: 438-446
NAID
Related Report
Peer Reviewed
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