MiR-30b-5p promotes myocardial cell apoptosis in rats with myocardial infarction through regulating Wnt/β-catenin signaling pathway.

Abstract

The aim of this study was to screen differentially expressed microribonucleic acids (miRNAs) in the heart tissues of rats with myocardial infarction (MI), to explore the relationship between miR-30b-p and MI, and to further research the action mechanism of miR-30b-p. Rat MI models were established. Then 3 rats in experimental (MI) group and 3 rats in sham operation (Sham) group were selected, RNAs were extracted from heart tissues, and differentially expressed miRNAs in the two groups were screened using transcriptome sequencing techniques. TargetScan (http://www.targetscan.org/vert_80/) was applied to predict miR-30b-5p target genes, which then were collected and subjected to enrichment analysis conducted using Metascape (Metascape, Berlin, Germany). Myocardial cells were extracted from MI rats and transfected with miR-30b-5p inhibitor. Then the changes in cell proliferation and apoptosis were detected by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-diphenytetrazoliumromide (MTT) assay and flow cytometry, respectively. The expressions of β-actin, β-catenin, Caspase-3 and cleaved Caspase-3 were detected in myocardial cells transfected with miR-30b-5p via Western blotting (WB). A total of 85 differentially expressed miRNAs were detected in the heart of MI rats, and miR-30b-5p expression was down-regulated (P<0.01). In addition, target genes regulated by miR-30b-5p participated in the vascular development, miRNA metabolic process and Wnt signaling pathway. In comparison with miR-negative control (NC) transfection, miR-30b-5p inhibitor transfection promoted the proliferation of myocardial cells but inhibited their apoptosis (P<0.05). Compared with those in miR-NC transfection group, the expressions of β-catenin and cleaved Caspase-3 proteins were down-regulated in miR-30b-5p inhibitor transfection group (P<0.01). MiR-30b-5p is involved in the proliferation and apoptosis of myocardial cells via regulating the Wnt/β-catenin signaling pathway, and it may become a potential target for the diagnosis of MI in clinic.