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Effect of lncRNA GAS5 on rats with acute myocardial infarction through regulating miR-21.

OBJECTIVE
The aim of this study was to investigate the effect of long non-coding ribonucleic acid (lncRNA) growth arrest specific 5 (GAS5) on acute myocardial infarction (AMI) model rats and to explore its regulatory mechanism.


MATERIALS AND METHODS
The rat model of AMI was established by subcutaneous injection of isoproterenol (ISO). 30 Sprague Dawley (SD) rats were randomly divided into three groups, including Control group, Model group, and lncRNA GAS5 inhibitor [small interfering ribonucleic acid (siRNA) GAS5] group. Hematoxylin and eosin (H&E) staining was used to detect the pathological damage of myocardial tissues in rats of each group. Myocardial cell apoptosis in each group determined via terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The levels of matrix metalloproteinase (MMP)-2 and MMP-9 in the serum of rats in each group were examined by enzyme-linked immunosorbent assay (ELISA). Reverse transcription-polymerase chain reaction (RT-PCR) was adopted to measure the expression level of miR-21 in rat myocardial tissues.


RESULTS
Compared with Control group, rats in Model group had significantly poor cardiac function, serious pathological damage of myocardial tissues, as well as increased apoptosis rate of myocardial cells. Meanwhile, the levels of MMP-2 and MMP-9 were significantly elevated in serum of Model group, while miR-21 level was down-regulated. In comparison with Model group, rats in siRNA GAS5 group exhibited significantly improved cardiac function, alleviated pathological damage to myocardial tissues, as well as decreased apoptosis rate of myocardial cells. Furthermore, the levels of MMP-2 and MMP-9 decreased significantly in serum of siRNA GAS5 group, whereas the expression level of miR-21 in myocardial tissues was down-regulated.


CONCLUSIONS
SiRNA GAS5 can enhance the cardiac function of AMI model rats, relieve pathological damage, reduce myocardial cell apoptosis, and inhibit the occurrence of myocardial fibrosis. The possible underlying mechanism may be associated with up-regulation of miR-21.