MALAT1 lncRNA Induces Autophagy and Protects Brain Microvascular Endothelial Cells Against Oxygen–Glucose Deprivation by Binding to miR-200c-3p and Upregulating SIRT1 Expression

•MALAT1 and autophagy were upregulated by oxygen–glucose deprivation in brain microvascular endothelial cells.•MALAT1 upregulated SIRT1 by inhibiting miR-200c-3p expression.•MALAT1-miR-200c-3p-SIRT1 regulatory axis promotes brain microvascular endothelial cells’ autophagy and survival. There is growing evidence that long noncoding RNAs (lncRNAs) play important roles in various biological processes. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is one of the most highly upregulated lncRNAs in cerebral ischemia. However, the molecular mechanism of MALAT1 during cerebral ischemia is still unclear. This experiment is intended to investigate the role of MALAT1 in cerebral ischemia and its relationship with autophagy. Oxygen–glucose deprivation (OGD) in brain microvascular endothelial cells (BMECs) was used to mimic ischemic-like conditions in vitro. Real-time PCR, MTT, LDH assay and western blot were used to evaluate the levels of MALAT1, miR-200c-3p, SIRT1, cell survival and proteins. We found that the expression of MALAT1 and LC3BII were upregulated and p62 was downregulated by OGD. Inhibition of MALAT1 attenuated the autophagy activation and promoted cell death. We further revealed that MALAT1 downregulated the expression of miR-200c-3p by directly binding to miR-200c-3p. Furthermore, miR-200c-3p inhibited the autophagy and survival in BMECs by binding to 3′UTR of SIRT1, whereas MALAT1 overturned the inhibitory effect of miR-200c-3p. In conclusion, our study illuminated a novel Malat1-miR-200c-3p-SIRT1 pathway in the regulation of autophagy, in which, MALAT1 activates autophagy and promotes cell survival by binding to miR-200c-3p and upregulating SIRT1 expression.