2010 Fiscal Year Final Research Report
Antiapoptotic effect of glutaredoxin in myocardiac cellsb induced by regulationg the redox state of GAPDH.
| Project/Area Number |
21890193
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Nagasaki University |
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Principal Investigator |
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| Project Period (FY) |
2009 – 2010
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| Keywords | 酸化ストレス / 心筋保護 / 循環器・高血圧 |
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| Research Abstract |
It is known that NO induced S-nitrosylation of GAPDH elicits its nuclear translocation and causes apoptotic cell death. In H9c2-control cells, NO-induced cell death increased dose-dependently compare to GRX1-overexpressed rat myocardiac H9c2 cells(H9c2-GRX). We revealed that GRX1 suppressed S-nitrosylation of GAPDH in H9c2-GRX. In addition, NO-induced nuclear translocation of GAPDH was decreased in H9c2-GRX compared to H9c2 control cells. These data suggest that GRX exerts the antiapoptotic effect by suppressing the S-nitrosylation of GAPDH.
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