Effect of TGF-β on WT1 expression in podocyte.
| Project/Area Number |
23790930
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | Gunma University |
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Principal Investigator |
SAKAIRI Toru 群馬大学, 医学部, 助教 (20455976)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 糖尿病性腎症 / 巣状糸球体硬化症 / 糸球体上皮細胞 / TGF-beta1 / WT1 / TGF-beta / Wilms tumor 1 / TGF-beta 1 / podocyte |
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| Research Abstract |
TGF-beta1 is involved in diabetes nephropathy and focal segmental glomerulonephritis. Transcriptional factor Wilms tumor suppressor gene (WT1) is essential for normal function of podocytes. We found that TGF-beta1 reduces WT1 expression in both cultured humanpodocytes and mouse podocytes. Using the cultured podocytes, we identified following mechanisms by which TGF-beta1 suppress WT1 expression. First, Smad4 mediates a decrease in WT1 expression by TGF-beta1. Second, TGF-beta1 caused DNA methylation in promoter region of the podocytes. Our results indicate that diverse pathways contribute to the TGF-beta1-induced WT1 reduction that may result in podocyte injury.
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Report
(3 results)
Research Products
(15 results)
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[Presentation] A Novel Case of Nephrotic Syndrome Caused by Immune-Mediated Severe LCAT Deficiency.2011
Author(s)
Takahashi S, Hiromura K, Tsukida M, Ohishi Y, Hamatani H, Sakurai N, Sakairi T, Ikeuchi H, Maeshima A, Kuroiwa T, Nagata M, and Nojima Y.
Organizer
The 44th Annual Meeting of the American Society of Nephrology
Place of Presentation
Philadelphia, USA
Related Report
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