Rong Yang1,
Yujuan Shi1,
Wanfang Yang1,
Qun Zeng1,
Guoyi Zhao1 and
Xiaoliang Wang2
2Center for Cardiovascular Sciences, Albany Medical Center, Albany, NY 12208, USA
Abstract Apoptosis is a crucial mode of cell death induced by ischemia and reperfusion, and ischemic postconditioning (PostC) has been reported to inhibit cell apoptosis. Inducible nitric oxide synthase (iNOS) has been confirmed to play an important role in triggering and mediating the late cardio-protection against ischemia/hypoxia. In this study, we found that hypoxic PostC remarkably up-regulated the expression of iNOS and decreased cardiomyocyte apoptosis. Pre-treatment with 1400w (a highly selective inhibitor of iNOS) or iNOS siRNA weakened the anti-apoptotic effect of hypoxic PostC. These findings suggested that iNOS may be one of the key molecular mechanisms responsible for the inhibition of apoptosis by hypoxic PostC.
Keywords inducible nitric oxide synthase; hypoxic postconditioning; apoptosis; cardiomyocyte
Received 2014-12-2
Accepted 2015-4-10
Funding This work was supported by the grants from the National Natural Science Foundation of China (Nos. 81100150 and 81170144), and the Natural Science Foundation of Shanxi Province (No. 2012011040-1).
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