| Project/Area Number |
24591569
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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 | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SEKINE Takashi 東邦大学, 医学部, 教授 (50255402)
IGARASHI Takashi 独立行政法人国立成育医療研究センター, 総長 (70151256)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 小児腎・泌尿器学 / ネフローゼ症候群 / 腎臓疾患 / 遺伝学 / ネフローゼ / 蛋白尿 / 巣状糸球体硬化症 / MYH9 |
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| Outline of Final Research Achievements |
It remains to be elucidated how idiopathic nephrotic syndrome including focal segmental glomerulosclerosis (FSGS) develops, while glomerular podocyte cytoskeletal proteins have recently emerged as candidate molecules associated with development of proteinuria. Mutations in the MYH9 gene, which encodes nonmuscle myosin heavy chain-IIA (NMMHC-IIA), cause Epstein syndrome and secondary FSGS in the kidney.
Firstly, we showed that NMMHC-IIA was localized at primary processes of the podocyte. Secondly, podocyte expression of NMMHC-IIA decreased specifically in Epstein syndrome and idiopathic nephrotic syndrome including primary FSGS. Thirdly, expression of other podocyte-associated proteins did not significantly changed in both FSGS and other chronic glomerulonephritis. These results suggest that NMMHC-IIA is strongly associated with development of idiopathic nephrotic syndrome, playing a pivotal role in maintenance of podocyte cytoskeleton.
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