Structure-function association in podocytopathy via Rho family small G proteins
| Project/Area Number |
26670427
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | Juntendo University |
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Principal Investigator |
Nagase Miki 順天堂大学, 医学(系)研究科(研究院), 准教授 (60302733)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ポドサイト傷害 / Rac1 / アクチン細胞骨格 / 細胞の運動性 / 低分子量G蛋白質 / 鉱質コルチコイド受容体 / マクロファージ / 心筋細胞 / Ｒａｃ１ / ポドサイト障害 / オプトジェネティクス / 細胞骨格 / アクチン |
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| Outline of Final Research Achievements |
Rac1, a Rho family small GTPase, is a multi-functional molecule that controls cytoskeleton, oxidative stress, gene transcription, and cell motility, in a cell-specific manner. In this study, we analyzed the role of Rac1 in the pathobiology of glomerular podocytes, focusing on the structure-function association, and compared its roles in other cells. In podocytes, both Rac1 hyperactivation and hypoactivation resulted in podocyte injury, albuminuria, and glomerulosclerosis, and affected actin cytoskeleton and cell motility by distinct mechanisms. Macrophage Rac1 played a central role in lipopolysaccharide-evoked acute kidney injury through M1 cytokine production. Cardiomyocyte Rac1 contributed to the pressure overload-induced heart failure via induction of NOX4.
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Report
(3 results)
Research Products
(17 results)
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[Presentation] 食塩と高血圧2015
Author(s)
長瀬美樹
Organizer
第38回日本高血圧学会総会
Place of Presentation
愛媛
Year and Date
2015-10-11
Related Report
Invited
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