| Project/Area Number |
22590897
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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 | Saitama Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Tsutomu 埼玉医科大学, 医学部, 講師 (30406475)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
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| Keywords | 老化 / NFkB 経路 / 線維化 / 遺伝子改変動物 / 尿細管上皮細胞 / NFkB / 腎線維化 / 線維芽細胞 / ポドサイト / NFkBシグナル / 糸球体硬化 |
|---|
| Research Abstract |
We generated genetically-modified mice, gGT.Cre:IkBdN mice, in which the NFkB pathway is blocked exclusively in tubular epithelium. In the kidney of wild-type mice at 20 month-old, peritubular fibrosis was observed compared to those at 3 moth-old, which seemed to be an age-related, histological change. In contrast, peritubular fibrosis was significantly enhanced in the kidney of gGT.Cre:IkBdN mice at 20 month-old. Therefore, long-term blockade of NFkB pathway in tubular epithelium was supposed to accelerate renal fibrogenesis.
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