| 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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| 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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