2013 Fiscal Year Final Research Report
Antiapoptotic effect of glutaredoxin in cardiomyocytes by inducing changes in the cellular redox system.
| Project/Area Number |
23791715
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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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) |
2011 – 2013
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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 glutaredoxin (GRX) protects cells from oxidative stress by regulating the redox state of certain proteins. In GRX1-overexpressed rat myocardiac H9c2 cells (H9c2-GRX), nitric oxide (NO)-induced apoptosis and decreasing of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity was suppressed compare to H9c2-control cells (H9c2-control). Furthermore, under NO stimulation, nuclear translocation of GAPDH and S-nitrosylation of protein was suppressed in H9c2-GRX compare to H9c2-control. These data suggest that the overexpression of GRX1 could protect cardiomyocytes against NO-induced apoptosis, likely through the inhibition of the oxidative modification and the nuclear translocation of GAPDH.
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