| Project/Area Number |
10670986
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
KUWAHAWA Michio Tokyo Medical and Dental University, School of Medicine, Lecturer, 医学部, 講師 (60221230)
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| Co-Investigator(Kenkyū-buntansha) |
SASAKI Sei Tokyo Medical and Dental University, School of Medicine, Associate Professor, 医学部, 助教授 (60170677)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | glucocorticoid / cell cycle / mesangial cell / nitric oxide / AQP2 / molecular biology / C. elegans / 水チャネル |
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| Research Abstract |
1. We examined the intracellular mechanism of glucocorticoids action using mesangial cells and an experimental model of anti-GBM nephritis. Our results suggest that glucocorticoids stimulate p21CIP1 gene promoter activity and cause cell cycle arrest. This action may be associated with the effectiveness of glucocorticoids in the treatment of glomerulonephritis.
2. We investigated the intracellular signal transduction pathways to clarify the pathogenesis of glomerulonephritis. New findings are ; 1) inducible nitric oxide synthase is induced in the absence of active NF-kB, 2) p27Kip1 and p21CIP1, cell cycle inhibitors, cause cell hypertrophy, and 3) TGF-β-activating kinase-1 inhibits cell cycle and expression of cyclin D1 and A.
3. We reported a case of autosomal dominant nephrogenic diabetes insipidus that is cased by a deletion of seven bases in the AQP2 gene (809del 7). We found that this mutation causes an inhibition of transcription or a trafficking defect.
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