| Project/Area Number |
24591188
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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 | Gunma University |
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Principal Investigator |
HIROMURA Keiju 群馬大学, 医学(系)研究科(研究院), 准教授 (70292597)
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| Co-Investigator(Renkei-kenkyūsha) |
SAKAIRI Toru 群馬大学, 大学院医学系研究科, 助教 (20455976)
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| Research Collaborator |
STUART Shankland University of Washington, Division of Nephrology, Professor
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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: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ボウマン嚢上皮細胞 / 糸球体障害 / sestrin 2 / mTOR経路 / ネフローゼ症候群 / 蛋白尿 / 国際情報交換 / 国際情報交換 米国 |
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| Outline of Final Research Achievements |
In the current study, we have shown that sestrin 2, a novel stress-inducible protein, is selectively expressed Bowman's epithelial cells of normal rat kidney. In rat model of nephrotic syndrome (minimal change or focal segmental glomerulosclerosis) and crescentic glomerulonephritis, sestrin 2 expression was decreased, demonstrating that decreased expression of Sestrin 2 could be a novel marker of Bowman’s epithelial cell injury. In addition, mTOR pathway, which is the downstream of target of sestrin 2, was up- or down-regulated by the changes of sestrin 2 expression, suggesting that sestrin 2-mTOR pathway could be a target of treatment for glomerular injury.
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