Investigation of the role of Rac/MR cascade in various experimental nephropathy : its target cells and underling mechanism
| Project/Area Number |
24790835
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2012 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ミネラルコルチコイド受容体 / Rac1 / アルドステロン / 糖尿病性腎症 / 肥満 / 脂肪細胞 |
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| Research Abstract |
Our study suggested that increased plasma aldosterone and local Racl activation in the kidneys cooperatively activates MR and strongly develops renal impairment in obesity-related diabetic model mice. Glucose stimulation activates Racl and MR in cultured mesangial cells. Since Racl inhibition completely suppresses MR activation by glucose, it is suggested that glucose activates MR via Rac1. Cultured medium of fat cells isolated from obese rat strongly stimulates aldosterone secretion of the cultured adrenal cortex cells, and it suggests the fat cell derived aldsterone releasing factor and its increase in obesity.
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Report
(3 results)
Research Products
(3 results)
