| Project/Area Number |
11671057
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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 WOMEN'S MEDICAL UNIVERSITY |
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Principal Investigator |
BABAZONO Tetsuya TOKYO WOMEN'S MEDICAL UNIVERSITY SCHOOL OF MEDICINE, ASSISTANT PROFESSOR, 医学部, 講師 (70208718)
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| Co-Investigator(Kenkyū-buntansha) |
HIRAYAMA Michiyo TOKYO WOMEN'S MEDICAL UNIVERSITY ASSISTANT, 医学部, 助手 (60297512)
TAKEDA Masanobu TOKYO WOMEN'S MEDICAL UNIVERSITY ASSISTANT, 医学部, 助手 (80277110)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Diabetic Nephropathy / Protein kinase C / Renin-angiotensin system / Hyaluronic acid / 糖尿病性賢症 / レニン・アンギオテンシン / レニン.アンギオテンシン系 / MAPキナーゼ |
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| Research Abstract |
To clarify the effects of protein kinase C in the pathogenesis of diabetic nephropathy, we conducted an animal study using streptozotocin-induced diabetic rats and in vitro study on cultured mesangial and renal interstitial fibroblast.
1) In streptozotocin-induced diabetic rat glomeruli, in situ FKC activity and specific PKC isoform expression were increased compared with nonnal rat glomeruli.
2) Both high glucose and angiotensin II increased PKC activity in cultured mesangial cells.
3) High glucose increased hyaluronal production by renal interstitial fibroblasts through the PKC-TGF-β cascade.
These results suggest that PKC is upregulated not only in mesangial cells but also renal interstitial fibroblasts in diabetes. PKC activation in diabetic kidney is at least in part through intrarenal angiotensin II.
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