1998 Fiscal Year Final Research Report Summary
Basic investigation for the pathogenesis of renal disease ; search for intervention based on pathophysiology
| 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)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Mesangial cells / extracellular matrix / anti-thy1 / glomerulonephritis / chloride blocker / glomerular epithilial cell / complement regulatory protein / SCR motive |
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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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[Publications] Hori, Y., S.Kaname, M.Hirakata, N.Joki, M.Fukagawa, T.Okuda, K.Miyazono, T.Katoh, T.Fujita and K.Kurokawa: "Mechanical stretch enhances latent TGF-beta binding protein-1 (LTBP-1) expressin in cultured rat mesangial cells" 30th.Am.Soc.Nephrol.meeting, San Antonio. (1997)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Hori Y,Yamada K,Hanafusa N,Okuda T,Okada N,Miyata T,Couser WG,Kurokawa K,Fujita T,Nangaku M: "Crry, a complement regulatory protein, modulates renal interstitial disease induced by proteinuiria." (Submitted).
Description
「研究成果報告書概要(欧文)」より
