| Project/Area Number |
09557088
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Kidney internal medicine
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| Research Institution | University of Tokyo |
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Principal Investigator |
OKUDA Toshihiro University of Tokyo, Health service center, assistant professor, 保健管理センター, 助手 (80177170)
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| Co-Investigator(Kenkyū-buntansha) |
NANGAKU Masaomi University of Tokyo, 1st.Department of Internal Medicine, assistant professor, 医学部(病), 助手
UMEZU Michio University of Tokyo, 1st.Department of Internal Medicine, assistant professor, 医学部(病), 助手 (70292935)
深川 雅史 東京大学, 医学部・附属病院, 医員
堀 雄一 東京大学, 医学部・附属病院, 医員
野入 英世 東京大学, 医学部・附属病院, 医員
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥11,600,000 (Direct Cost: ¥11,600,000)
Fiscal Year 1998: ¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1997: ¥7,900,000 (Direct Cost: ¥7,900,000)
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| Keywords | Mesangial cells / extracellular matrix / anti-thy1 / glomerulonephritis / chloride blocker / glomerular epithilial cell / complement regulatory protein / SCR motive / 腎障害 / CD59 / antisense / 内皮細胞障害 / 間質障害 / メサンギウム細胞 / Thy-I腎炎 / 上皮細胞障害 / 細胞外基質 |
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| Research Abstract |
(1) Histological amelioration was observed in anti thy-1 antibody induced glomerulonephritis model when Cl channel blocker (IAA-97) was given to the experimental animals (rats). This observation suggests the possibility that progression of glomerulonephritis is suppressed by Cl channel blocker. (2) It was observed that Cl channel blocker suppresses the extracellular matrix production at mRNA level. (3) The important role of complement was proved in a new glomerulonephritis model caused by anti-epithelial cell antibody, which leads to intraglomerular thrombosis and renal failure. (4) Addition of antibody to CD59, complement regulating protein expressed in this new *lomerulonephritis model, exacerbates glomerular injury, indicating protective effects of CD59. (5) Intrarenal perfusion of antisense oligodeoxynucleotide to complement regulatory protein via renal artery suppressed resulted in both suppression of complement regulatory protein expression and exacerbation of tubulointerstitial injury caused by proteinuria. This observation indicates complement present in proteinuria injures tubular cells in a complement dependent way, which could be reversed by complement regulatory protein. (6) A novel complement regulatory protein which have the same SCR motive as other complement regulatory proteins was obtained.
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