Abstract
The current study mainly aimed to evaluate the expression and the potential mechanism of miR-29a-3p in the hearts of mice after cardiac ischemia reperfusion (CIR) injury. Quantitative PCR was carried out to assess the relative levels of miR-29a-3p in the hearts of a CIR injury mouse model. To the best of our knowledge, the current study is the first to show that the level of miR-29a-3p was significantly decreased in the hearts of CIR injury mouse models compared with that of sham controls. Moreover, the authors found that decreased miR-29a-3p levels enhanced the production of reactive oxygen species in cardiomyocytes. Meanwhile, the inhibition of miR-29a-3p induced substantial cardiomyocyte apoptosis. Further study showed that the inhibition of miR-29a-3p decreased the activation of Akt and p38, suggesting a stress-induced self-regulatory mechanism after CIR injury in primary cardiomyocytes. A dual luciferase assay and western blot analysis showed that Bax was a target gene of miR-29a-3p. The authors also measured the level of miR-29a-3p in the plasma of 100 acute myocardial infarction (AMI) patients and found that circulating miR-29a-3p was significantly decreased in AMI patients. Receiver operating characteristic curve analysis showed that miR-29a-3p could be used to screen AMI patients from healthy controls. Hence, the authors of the current study propose that reduced miR-29a-3p levels in primary cardiomyocytes contribute to CIR injury-related apoptosis mainly by targeting Bax.