MiR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression

Abstract

The aim of the present study was to evaluate the functional association between the expression of miR-483-3p and acute myocardial infarction (AMI) in patients and in vitro. H9c2 cells were incubated in a vacuum with 5% CO2, 5% H2 and 90% N2 for 2 h, which generated the AMI model in vitro. Reverse transcription-quantitative polymerase chain reaction was used to measure miR-483-3p expression, and flow cytometry analysis and ELISA analysis were used to analyze apoptosis rate via caspase-3 and caspase-9 activity kits. B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) and transcriptionally suppressed the protein expression of insulin growth factor 1 (IGF-1) were analyze using western blot analysis. The results demonstrated that the expression of miR-483-3p in patients with AMI was increased when compared with the control group. In the in vitro model, the overexpression of miR-483-3p promoted apoptosis, increased caspase-3 and caspase-9 activity levels, induced the protein expression of Bcl-2/Bax and IGF-1. Picropodophyllotoxin, an IGF-1 inhibitor, was administered to cells following the overexpression of miR-483-3p. Administration of picropodophyllotoxin suppressed IGF-1 protein expression, promoted apoptosis, increased caspase-3 and caspase-9 activity levels, and induced the protein expression of Bax/Bcl-2. The results of the present study revealed that miR-483-3p may regulate AMI via the IGF-1 signaling pathway and may support the restoration of functional performance following AMI.