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.
Keywords: microRNA-483-3p; acute myocardial infarction; apoptosis; insulin growth factor 1.