Expression of miR-223-3p in a rat model of myocardial infarction and the effects of miR-223-3p on cardiomyocytes

Abstract

ABSTRACT This study aimed to investigate the expression of miR-223-3p in a rat model of myocardial infarction and the effects of miR-223-3p on cardiomyocytes. Forty rats were randomly divided into mock surgical, model (acute myocardial infarction (AMI) group (AMIG)), AMI + miR-223-3p adenovirus (intervention group (IG)), and AMI + scramble-NC (negative control group (NCG)) groups. Cardiac function was assessed by small animal echocardiography. Reverse transcription polymerase chain reaction was used to quantify the expression of miR-223-3p. The expression levels of miR-233-3p and SOX6 mRNA in the blank control group (BCG) and mock surgical group (MSG) were lower than those in the AMIG, IG, and NCG (P < 0.05), while the cardiac function indices of the BCG and MSG were higher than those of the AMIG, IG, and NCG (P < 0.05). The expression levels of miR-233-3p and SOX6 mRNA in the AMIG and NCG were significantly higher than those in the IG, while their cardiac function indices were significantly lower than those in the IG. Our findings indicate that the silencing of miR-223-3p effectively improves the cardiac function of rats, and the overexpression of miR-223-3p promotes the apoptosis of cardiomyocytes. Thus, miR-223-3p may be a new therapeutic target for AMI.