MiR-124 attenuates angiogenesis via the p38/MAPK and PI3K/AKT signaling pathways in acute myocardial infarction

Due to its rapid onset and high mortality, acute myocardial infarction (AMI) is considered as one of the most fatal diseases among heart diseases. Therefore, exploring its potential pathogenesis and developing effective treatment approaches for AMI have become a research hotspot in the medical community. In the present study, clinical blood samples from patients with AMI were analyzed and the results showed that the expression of microRNA (miR)-124 was significantly increased in peripheral blood of patients with AMI compared with healthy subjects. In addition, miR-124 overexpression notably promoted the apoptosis of HUVECs and attenuated their proliferative ability. Based on these findings, RNA from HUVECs was extracted and sequenced to investigate the changes in the gene expression profile triggered by miR-124 overexpression. The upregulated genes were enriched in several signaling pathways such as PI3K/AKT, while the downregulated ones were mainly enriched in metabolic-related signaling pathways. Additionally, the chromosomal location analysis revealed that the differentially expressed genes (DEGs) were distributed in all chromosomes, except the Y sex chromosome. Furthermore, the characteristic profile of DEGs mediated by miR-124 overexpression was analyzed via Connectivity Map analysis. The analysis revealed that anisomycin and sanguinarine, two agonists of the p38/MAPK signaling pathway involved in the inhibition of angiogenesis, exerted the highest enrichment scores. Additionally, Gene Set Enrichment Analysis demonstrated that DEGs were mainly enriched in the PI3K/AKT signaling pathway, thus inhibiting angiogenesis. Collectively, the present results indicated that miR-124 overexpression could promote AMI by affecting angiogenesis. Overall design: mRNA profile changes between mir124 over-expression huvec and normal huvec