| Project/Area Number |
26461225
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Kyoto University |
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Principal Investigator |
YOKOI HIDEKI 京都大学, 医学研究科, 講師 (90378779)
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| Co-Investigator(Kenkyū-buntansha) |
笠原 正登 奈良県立医科大学, 医学部, 研究教授 (50393351)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 糸球体腎炎 / 増殖因子 / 腎不全 / タンパク尿 / ノックアウトマウス / 腎臓病 / 炎症 / 細胞外基質 / 腎炎 / 腎臓 / TGF-β |
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| Outline of Final Research Achievements |
In this study, we induced anti-GBM glomerulonephritis in podocyte-specific CTGF knockout mice.These mice exhibited no improvement of proteinuria, crescentic formation, mesangial expansion and macrophage infiltration.
Therefore, we generated mesangial cell-CTGF knockout mice (Mes-CTGF cKO mice) using PDGFR-alpha-Cre mice. Mes-CTGF cKO mice showed reduction of crescentic formation, mesangial expansion, proteinuria, TGF-beta1, alpha-SMA, fibronectin and MCP1 expression. Infiltration of macrophages was also inhibited and the ratio of M1 macrophage/M2 macrophage was significantly reduced.
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