2002 Fiscal Year Final Research Report Summary
Functional analysis of complement regulatory proteins in glomerulonephritis and development of novel therapeutic approaches
| Project/Area Number |
13671100
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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 | The University of Tokyo |
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Principal Investigator |
NANGAKU Masaomi The University of Tokyo, School of Medicine, Assistant Researcher, 医学部附属病院, 助手 (90311620)
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| Co-Investigator(Kenkyū-buntansha) |
OKUDA Toshihiro The University of Tokyo, Institute of Hygiene, Assistant Researcher, 保健センター, 助手 (80177170)
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| Project Period (FY) |
2001 – 2002
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| Keywords | complement / complement regulatory protein / kidney failure / glomerulonephritis / proteinuria / renal tubular cell / gene transfer |
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| Research Abstract |
The aim of this project is to progress researches in complement and complement regulatory proteins and to develop novel therapeutic approaches based on the findings obtained during the process.
We elucidate a role of DAF, a membrane-bound complement regulatory protein, in glomeruli by inducing anti-glomerular basement membrane nephritis in DAF knock-out mice. We also clarified a pathogenic role of complement components hi proteinuria urine by investigating remnant kidney rats, which develop proteinuria and progressive renal failure. Our studies utilizing C6-deficient rats suggested that complements in massive non-selective proteinuria mediates progression of chronic renal failure by damaging the tubulointerstitium.
Based on these findings, we developed an adenovirus vector expressing recombinant soluble complement regulatory protein. Gene transfer of the vector protected the kidney from immune mediated renal injury.
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Research Products
(12 results)
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[Publications] Nangaku M, Miyata T, Sada T, Mizuno M, Inagi R, Ueda Y, Ishikawa N, Yuzawa H, Koike H, de Strihou Cv Y, Kurokawa K: "Anti-hypertensive agents inhibit in vivo the formation of advanced glycation end products and improve renal damage in a type 2 diabetic nephropathy"J Am Soc Nephrol. in press.
Description
「研究成果報告書概要(欧文)」より
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