Abstract
PurposeMyocardial ischemia-reperfusion injury (MIRI) is a common pathophysiological process after occlusion of the blood vessels to restore blood supply. Apoptosis is one of the ways of myocardial cell death in this process. MicroRNAs (miRNAs), a class of short and noncoding RNAs, are involved in multiple biological processes by post-transcriptionally targeting their downstream effectors. To date, whether miRNAs exert biological effects in myocardial ischemia-reperfusion (I/R) injury remains to be further studied.MethodsIn this study, we induced MIRI model by ligating rat left anterior descending artery (LAD) for 30 mins and reperfusion for 2 hrs. The differential expression profile of miRNAs in rat models of MIRI was analyzed by miRNAs sequencing.ResultsWe found that miRNAs sequencing analysis showed the expressions of 15 types of miRNAs, including miR-346, were downregulated and 29 types of miRNAs were elevated in the MIRI rat model. We observed the key regulator of apoptosis Bax was a predicted downstream target of miR-346 using online software TargetScan. And luciferase reporter assay was utilized to certify this prediction. Over-expression of miR-346 can attenuate myocardial injury and narrow infarct area by inhibiting myocardial cell apoptosis in rat models.ConclusionThis study revealed a novel pathway, miR-346/Bax axis, in the regulation of apoptosis in MIRI and which might be a new molecular mechanism and therapeutic target.
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