MIR-21 REGULATES EARLY MYOCARDIAL CELL APOPTOSIS AFTER ISCHEMIA-REPERFUSION THROUGH THE PTEN/AKT SIGNALING PATHWAY

Baihua Chou¹, Lijun Lee¹, Minfei Lee¹, Yuqing Sui¹, Changshan Zhang^{2, *}

¹Nanhai Hospital, Southern Medical University Carvascular Medicine, Foshan 528244, PR China - ²Department of Emergency Center, the Second Hospital of Yulin City, Yulin 719000, PR China

Objective: To investigate the mechanism of miR-21 in the regulation of myocardial cell apoptosis during early ischemia-reperfusion. 

Methods: 45 healthy, male Sprague-Dawley (SD) rats of a clean grade were selected for the sample in this study. 18 of the 45 SD rats were then randomly selected from the total sample; these rats were randomly divided into a control group and a miR-21 overexpression group, with 9 rats in each group. The rats in the control group were transfected with the blank control virus, and the rats in the miR-21 overexpression group were transfected with miR-21 mimics. The expressions of miR-21 and PTEN in the two groups of rats were determined by real-time quantitative PCR. The remaining 27 rats were randomly divided into a sham operation group, a model group, and a miR-21 overexpression group, with 9 rats in each group. Among these, the rats in the sham operation group were transfected with a blank control virus for 2 weeks, before thoracotomy and wire hanging; the rats in the model group were transfected with a blank control virus and treated with ischemia-reperfusion; and, after transfection with miR-21 mimics, the rats in the miR-21 overexpression group were treated with ischemia-reperfusion. Real-time fluorescence quantitative PCR was employed to determine the expression of miR-21 in each group. The expressions of Bax, Bcl-2, and caspase-3 in the rats were determined by immunohistochemistry and a western blot. The western blot was also utilized to determine the expressions of PTEN and p-AKT in the rats. 

Results: Compared with the control group, the expression level of miR-21 was significantly higher in the miR-21 overexpression group (P<0.01), while the expression level of PTEN was significantly lower. Compared with the sham operation group, the expression levels of miR-21, Bcl-2/Bax, and p-AKT in the model group were significantly lower, while the expression levels of Bax, Bcl-2, caspase-3, and PTEN in the model group were significantly higher (P<0.05). Compared with the model group, the expression levels of miR-21, Bcl-2/Bax, and p-AKT were significantly higher in the miR-21 overexpression group, while the expression levels of Bax, Bcl-2, caspase-3, and PTEN were significantly lower (P<0.05). 

Conclusion: The upregulation of miR-21 expression may inhibit early myocardial cell apoptosis by activating the PTEN/AKT signaling pathway.