| Project/Area Number |
11671030
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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 | UNIVERSITY OF TOKYO |
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Principal Investigator |
NANGAKU Masaomi UNIVERSITY OF TOKYO SCHOOL OF MEDICINE, ASSISTANT, 医学部・附属病院, 助手 (90311620)
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| Co-Investigator(Kenkyū-buntansha) |
OKUDA Toshihiro UNIVERSITY OF TOKYO HEALTH SERVICE CENTER, ASSISTANT, 保健センター, 助手 (80177170)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1999: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | GLOMERULONEPHRITIS / KIDNEY FAILURE / COMPLEMENT / COMPLEMENT REGULATORY PROTEIN / PROTEINURIA / RENAL TUBULES / NEPHROTIC SYNDROME / MESANGIUM |
|---|
| Research Abstract |
Complement activation plays a critical role in the pathogenesis of many forms of glomerulonephritis. Complement activation also leads to progressive tubulointerstitial damage and eventual kidney failure. Recent advances have disclosed the mechanisms of regulation of complement activation by discovery of a number of complement regulatory proteins.
We demonstrated that a complement regulatory protein, Crry, in tubules protect tubulointerstitium from inappropriate complement activation in proteinuric urine, utilizing in vivo antisense approach.
We also showed that a soluble complement regulatory protein, clusterin, is up-regulated in mesangial cells by immune injury.
Recombinant complement regulatory proteins can be a valuable tool to treat kidney disease. We developed adenoviral vector to overexpress a soluble complement regulatory protein, sCrry. The product of the transgene was functionally active in vitro. In vivo gene transfer of vectors to inhibit inappropriate complement activation should be pursued.
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