| Project/Area Number |
23591586
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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 |
Pediatrics
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| Research Institution | Toho University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KUNISHIMA Shinji 独立行政法人国立病院機構(名古屋医療センター臨床研究センター), 臨床研究セーター, 室長 (60373495)
KURIHARA Hidetake 順天堂大学, 医学部, 准教授 (80311976)
MIURA Kenichiro 東京大学, 医学部附属病院, 助教 (70408483)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 巣状糸球体硬化症 / myosin IIA / ポドサイト / 蛋白尿 / 細胞骨格タンパク / podocyte / FSGS / 細胞骨格 / MYH9 / ネフローゼ症候群 / 細胞骨格分子 / foot process / NMMHC-IIA / proteinuria |
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| Research Abstract |
To lucidate the pathophysiology of nephrotic syndrome, especially FSGS, we investigated myosin IIA. First, We determined the precise localization of myosin IIA; myosin IIA is located at the primary process and cell body of podocye. In human kidney diseases manifesting heavy proteinuria, only in the kidney specimen from the patients with FSGS, the level of expression o myosin IIA was decreased, while in those from other kidney disease patients were not changed. In rat PAN nephrosis model, the expression level of myosin IIA was decreased at day 11 when heavy proteinuria was observed. Taken together, myosin IIA play the very important role in the development of human idiopathic nephrotic syndrome, especially FSGS.
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