MiR-489 aggravates H(2)O(2)-induced apoptosis of cardiomyocytes via inhibiting IGF1

Myocardial infarction (MI) is a major type of cardiovascular disorder worldwide. In the present study, we established a new microRNA (miRNA)–mRNA cross-talk network by integrating data obtained from The National Center for Biotechnology Information Gene Expression Omnibus (NCBI GEO). In addition, functional assays, including Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) analyses, were conducted using the Database for Annotation, Visualization, and Integration Discovery (DAVID). In our study, we generated a new differentially expressed miRNA (DEmiRNA)-differentially expressed gene (DEG) cross-talk network of MI composed of three miRNA (miR-489, miR-375, and miR-142-3p) nodes and 163 mRNA nodes. In vitro experiments demonstrated that miR-489 expression was increased in H(2)O(2)-treated H9c2 cardiomyocytes in vitro, mimicking myocardial injury. We observed that down-regulation of miR-489 reduced H(2)O(2)-induced apoptosis, while overexpression of miR-489 had the opposite effects, as revealed by flow cytometry and Western blot analyses. Furthermore, we confirmed the relationship between miR-489 and IGF1 through double luciferase reporter gene assays, which partly explains the antiapoptotic mechanism of miR-489. In conclusion, the experimental results of the present study could provide important clues for investigating the mechanism of MI.