Long non-coding RNA GAS5 reduces cardiomyocyte apoptosis induced by MI through sema3a

Abstract

ObjectiveTo investigate the role of GAS5 on cardiomyocyte apoptosis. MethodsMyocardial infarction (MI) model was established by the left-anterior descending coronary artery ligation. Norepinephrine (NE) was used to induce cardiomyocyte apoptosis. GAS5 levels and mRNA expressions of Semaphorin 3a (sema3a) were measured by qRT-PCR. Protein level of sema3a was detected by Western blotting. Cardiomyocyte apoptosis was detected by flow cytometry assay. RNA pull-down and RIP assay were used to verify the combination between GAS5 and sema3a. Infarct size was measured by TTC staining. ResultsGAS5 expression was increased in infarct boundary zone of MI group, while sema3a protein expression was decreased. Moreover, GAS5 expression in cardiomyocyte induced by NE was higher than control group, while sema3a protein expression was lower than control group. In addition, GAS5 could negatively regulate sema3a protein expression. pcDNA-GAS5 reversed cardiomyocyte apoptosis induced by NE, while pcDNA-sema3a countered the inhibitory effect. In animal experiment, overexpression of GAS5 decreased sema3a protein expression and reduced infarct size. ConclusionGAS5 could ameliorate cardiomyocyte apoptosis induced by MI via down-regulating sema3a.