1996 Fiscal Year Final Research Report Summary
Molecular biological analysis of the mechanism of acute renal failure
| Project/Area Number |
07457242
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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 | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Kumamoto University |
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Principal Investigator |
TOMITA Kimio Kumamoto University, School of Medicine, Professor, 医学部, 教授 (40114772)
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| Co-Investigator(Kenkyū-buntansha) |
KITAMOTO Yasunori Kumamoto University, School of Medicine, Associate Professor, 医学部, 講師 (80195297)
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| Project Period (FY) |
1995 – 1996
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| Keywords | acute renal failure / gene / glomerulus / tubules / endothelin / receptor |
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| Research Abstract |
We investigated the expression and regulation of endothelin-1 protein and mRNA,endothelin converting enzyme protein and mRNA,A type endothelin receptor mRNA,B type endothelin receptor mRNA in ischemic and cyclosporine-induced acute renal failure. Endothelin-1 mRNA started to increase from 30 minutes to several hours after ischemic insult or cyclosporine administration. A type endothelin receptor mRNA decreased in both types of acute renal failure. B type endothelin receptor mRNA increased in ischemic acute renal failure. However, it decreased in cyclosporine-induced acute renal failure. Endothelin converting enzyme protein and mRNA decreased in cyclosporine-induced acute renal failure. To elucidate the mechanism of inhibition of endothelin converting enzyme protein and mRNA,regulation of endothelin converting enzyme was investigated in cultured endothelial cells. Endothelin-1 has an inhibitory effect on endothelin converting enzyme protein and mRNA through B type endothelin receptor. These data suggests that impairments of renal function may be protected by the decrease in A type endothelin receptor and increase in B type endothelin receptor in ischemic acute renal failure. As for cyclosporine-induced acute renal failure, impairments of renal function may be protected by the decrease in A type endothelin receptor and decrease in endothelin converting enzyme through B type endothelin receptor.
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