Myocardial infarction (MI) is severe
heart disease leading to the death worldwide. Long noncoding RNAs (lncRNAs) play a vital role in progression of numerous
heart diseases. In the present study, we examined the effects of
lncRNA XIST and underlying mechanism on
hypoxia-induced apoptosis. In vitro model of MI was established by inducing
hypoxia in H9c2 cells.
CCK-8 assay was used to measure the cell viability in
hypoxia-induced H9c2 cells. The rate of cell apoptosis was assessed by using
caspase-3 assay. Transfection was carried out to upregulate the expressions of
lncRNA XIST, and miR-486-5p. RT-qPCR was used to measure the levels of
lncRNA XIST and miR-486-5p. Also, the relation between XIST and miR-486-5p was confirmed by using
Luciferase reporter assay. Our findings revealed that
hypoxia significantly downregulated the expressions of XIST. Also, the cell viability markedly increased due to the overexpression of XIST in
hypoxia-induced H9c2 cells, while overexpression of XIST significantly reduced the cell apoptosis in
hypoxia-induced H9c2 cells. On the other hand, opposite effects were observed due to the downregulation of XIST in
hypoxia-induced H9c2 cells. Moreover, XIST negatively regulated the expression of miR-4486-5p and upregulation of XIST inhibited hypoxic injury by downregulating miR-486-5p. Furthermore,
SIRT1 expression was negatively regulated by miR-486-5p. We concluded that
lncRNA XIST might provide protection against injury induced by
hypoxia via miR-486-5p/
SIRT1 axis.