| Budget Amount *help |
¥18,850,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥4,350,000)
Fiscal Year 2014: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥10,270,000 (Direct Cost: ¥7,900,000、Indirect Cost: ¥2,370,000)
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| Outline of Final Research Achievements |
To explore the precise physiological and pathophysiological implications of the slit diaphragm complex including a canonical member of transient receptor potential (TRP) channel TRPC6, in regulating the glomerular filtration function, we carried out detailed analysis with a minimally constructed slit-diaphragm-protein expression system and a ‘pseudo-slit diaphragm’ formed by podocytes on an artificial filter membrane. The results have suggested that the complex of TRPC6-podocin-(nephrin)-cytoskeletal actin mediates Ca influx into renal podocytes in response to receptor and mechanical stimuli, thereby effectively regulating the glomerular barrier function, and that conditions causing the excess of these Ca responses such as mutations associated with familial focal glomerulosclerosis and renal inflammation, may lead to disruption of the barrier and subsequent proteinuria.
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