Cardiomyocyte Apoptosis

XIST[LncRNA]

miR-873-5p[miRNA]

MCL1[mRNA]

H9c2 cells

Homo sapiens (human)

Eur Rev Med Pharmacol Sci. 2020 Dec;24(24):12878-12886. doi: 10.26355/eurrev_202012_24191.

Long noncoding RNA XIST regulates cardiomyocyte apoptosis by targeting miR-873-5p/MCL1 axis.

qRT-PCR;Western blot;

OBJECTIVE: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: LncRNA XIST can regulate cardiomyocyte apoptosis by targeting miR-873-5p.