| Project/Area Number |
07671235
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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 |
CHANG Hangil Univ.Tokyo, Health Servece Center, Assistant Prof., 保健管理センター, 助手 (30260524)
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| Co-Investigator(Kenkyū-buntansha) |
加藤 哲夫 東京大学, 医学部(分), 助手 (70194834)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Reanal failure / HGF / cytokine / gene therapy / adenuvirrus vector / 肝細胞増殖因子(HGF) / アデノウイルスベクター / HGF(Hepatocyte Growth Faetor) |
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| Research Abstract |
Our aim was to study the role of hepatocyte growth factor (HGF) in chronic renal failure patients and to explore the possibility of HGF as therapeutic agent in these patients. HGF was first purified and cDNA cloned by Nakamura et al. in Kyushu University as the agent to promote proliferation and differentiation of hepatocyte.
Subsequent studies have revealed that HGF has effects also in renal cells promoting proliferation and differentiation. Several investigators have reported HGF has beneficial effects in experimental models of acute renal failure. We have investigated the blood levels of HGF in chronic renal failure patients. In advanced renal failure patients requiring hemodialysis blood levels were increased. Since HGF is destructed almost exclusively in liver and urinary excretion is negligible, the observed increased in blood levels in these patients should be interpreted as HGF synthesis is increased in these patients. In order to specify the direct cause of increased HGF syntheses, we have further studied blood levels ofcytokines known to promote HGF synthesis in vitro. Blood levels of IL-1a, IL-1b, TNF,and injurin were not increased in these patients. Thus the reason why HGF levels is increased in chronic renal failure patients remained to be explained. We have extended our study to chronic renal failure patients with more renal reserve and had similar results. In another line of study, we have constructed adenovirus mediatted vector carrying HGF gene to investigate gene therapy in these patients. However, gene transfer efficiency in renaltissues was very small in experimental animals.
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