| Project/Area Number |
13557083
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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 | Institute for Molecular and Cellular Regulation, Gunma University |
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Principal Investigator |
KOJIMA Itaru Institute for Molecular and Cellular Regulation, Professor, 生体調節研究所, 教授 (60143492)
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| Co-Investigator(Kenkyū-buntansha) |
NOJIMA Yoshihisa Third Department of Internal Medicine, Gunma University, Professor, 医学部, 教授 (90201699)
張 有青 群馬大学, 生体調節研究所, 助手 (10302499)
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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 |
¥14,300,000 (Direct Cost: ¥14,300,000)
Fiscal Year 2002: ¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2001: ¥10,200,000 (Direct Cost: ¥10,200,000)
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| Keywords | follistatin / activin / regeneration medicine / renal tubular cell / apoptosis / growth factor / stem cell / epithelial cell / 腎尿細管 |
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| Research Abstract |
In the present study, we investigated the involvement of the activin-follistatin system in the regeneration of renal tubular cells after ischemia-reperfusion in rats. After ishcemia- reperfusion, the expression of the bA subunit of activin was markedly up-regulated. Histologically, immunoreactivity of activin A was increased in renal tubular cells after ischemia-reperfusion. In contrast, the expression of follistatin, an activin antagonist, was markedky reduced after ischemia-reperfusion. These results suggest that the effect of activin A becomes dominant after ischemia-reperfusion. To examine the role of activin A in this process, we administered follistatin immediately after reperfusion. Follistatin significantly improved histological derangements induced by ischemia-reperfusion. Thus, bleeding, monocytic infiltration and cast formation were markedly reduced by follistatin. Furthermore, the number of apoptotic cells was markedly reduced by follistatin. In addition, follistatin greatly incresed the number of BrdU-positive cells in renal tubule. In accoradance with these results, the serum BUN and creatinine levels were significantly reduced by the adminstartion of follistatin. These results indicate that activin A plays a critical role in the renal dysfunction after ischemia-reperfusion and adminstration of follistatin is effective in both reduction of tubular damages and promotion of tubular cell regeneration.
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