Abstract
The purpose of this study was to investigate the expression of miR-873-5p and long non-coding RNA X-inactive specific transcript (lncRNA-XIST) in myocardial infarction (MI), the interaction mechanism and the effect of target gene MCL1 on apoptosis in H9c2 cells. quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect and compare the expressions of miR-873-5p and lncRNA XIST in 8 myocardial infarction rats and 8 normal rats tissues, respectively, and the correlation between the expressions of miR-873-5p and lncRNA XIST in the myocardial tissues was explored. Next, qRT-PCR and Western blot were used to detect the effects of upregulation of miR-873-5p and downregulation of lncRNA XIST, as well as the impacts of their interactions on the expression level of MCL1 in H9c2 cells and the apoptosis of cells. It was found that the downregulation of miR-873-5p protected the heart against apoptosis after AMI, and lncRNA XIST inhibited apoptosis in H9c2 cells after hypoxia. Besides, inhibiting lncRNA XIST could upregulate miR-873-5p and downregulate MCL1, thus increasing apoptosis in the H9c2 cells after hypoxia. LncRNA XIST can regulate cardiomyocyte apoptosis by targeting miR-873-5p.
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