| 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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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 2002: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | complement / complement regulatory protein / kidney failure / glomerulonephritis / proteinuria / renal tubular cell / gene transfer / 炎症 / ノックアウトマウス |
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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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