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

Abstract

BACKGROUND: 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. METHODS: 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). RESULTS: 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). CONCLUSIONS: 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.