| Project/Area Number |
15K09247
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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 | Tokai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
川上 貴久 東京大学, 医学部附属病院, 助教 (10722093)
稲城 玲子 東京大学, 医学部附属病院, 特任准教授 (50232509)
南学 正臣 東京大学, 医学部附属病院, 教授 (90311620)
田中 哲洋 東京大学, 医学部附属病院, 講師 (90508079)
加藤 秀樹 東京大学, 医学部附属病院, 講師 (90625237)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 糸球体足細胞 / 蛋白尿 / 細胞骨格 / 高グルコース / TGF-β1 / 翻訳後修飾 / 糖尿病性腎症 |
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| Outline of Final Research Achievements |
We have carried out this project to determine the mechanisms of cytoskeletal derangement associated with metabolic stresses in podocytes leading to development and increase of proteinuria. In this project, we observed the changes in cytoskeletal architecture and migration of podocytes in response to several metabolic stress associated with diabetes. Interestingly, we found that altered expression of several cell cycle regulators were associated with those cellular changes. Moreover, our experimental data suggest that vitamin D might have a protective role against diabetic metabolic stresses through these pathways. We hope that novel therapeutic strategies against diabetic kidney disease will be developed by advance in this research project.
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