![Sample our Bioscience journals, sign in here to start your access, Latest two full volumes FREE to you for 14 days]({"type":"image" , "src" : "/sda/5925/TOC-Subject-Sample-2021-Bioscience.jpg"})
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.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
The data that support the findings of this study are openly available in figshare at http://doi.org/10.6084/m9.figshare.12301061.