| Project/Area Number |
09557089
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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 | 展開研究 |
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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 |
TANIGUCHI Shigeo The University of Tokyo, Hospital, Lecturer, 医学部・附属病院, 講師 (50188380)
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| Co-Investigator(Kenkyū-buntansha) |
NOIRI Eisei The University of Tokyo, Hospital, Assistant Professor, 医学部・附属病院, 助手 (00301820)
NAKAO Akihide The University of Tokyo, Hospital, Assistant Professor, 医学部・附属病院, 助手 (10159056)
OGATA Itsuro The University of Tokyo, Hospital, Assistant Professor, 医学部・附属病院, 助手 (80169169)
柳瀬 幹雄 東京大学, 医学部・附属病院, 医員
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥11,900,000 (Direct Cost: ¥11,900,000)
Fiscal Year 1998: ¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1997: ¥8,200,000 (Direct Cost: ¥8,200,000)
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| Keywords | Progression of renal injury / leukotriene B4 / ロイユトリエンB4 / 糸球体線維化 / 尿細管線維化 / type I collagen / type I procollagen C-proteinase enhancer protein |
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| Research Abstract |
It is well known that, whatever the underlying original disease, progressive renal injury is characterized by glomeruloscl erosisand tubulointerstitial fibrosis, which are the common pathological features of chronic renal failure. We have planned the present study to investigate the mechanism of fibrosis in the kidney.
First we examined the expression of type I procollagen C-proteinase enhnacer protein, PCPE, which was recently cloned by one of the investigators, Ogata I.By the same author PCPE has been to shown to play an important role in liver fibsosis. We have examined its expression in the kidney by Western blot analysis using cultured rat mesangial cells, normal rat kidney, and 5/6 nephrectomized rat kidney, and we could not detect its expression in the kidney. We also examined the expression of its mRNA by Northern blot analysis, and we could not detect it, neither. So we have concluded that PCPE plays minor role in the pathogenesis of renal fibrosis.
We also examined the role of leukotrine B4(LTB4)in the progression of renal diseases. We made hyperlipidemia-induced renal injury in rats, and treated these rats with LTB4 antagonist. This treatment markedly ameliorated kidney injury in these animals. Then we examined the distribution of leukotriene A4 hydrolase mRNA expression in rat nephronsegments, and found that it is present both in glomeruli and tubular segments. These result suggest the important role of LTB4 synthesized in the kidney in the pathogenesis of progressive renal injuries.
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