Ox-LDL-induced lncRNA MALAT1 promotes autophagy in human umbilical vein endothelial cells by sponging miR-216a-5p and regulating Beclin-1 expression.

Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) has been validated as a potent protective agent of Atherosclerosis (AS). Here, we explored the molecular mechanism of MALAT1 exerting protective function in oxidized low-density lipoprotein (ox-LDL)-stimulated human umbilical vein endothelial cells (HUVECs). qRT-PCR assay was used to assess the expression of MALAT1 and miR-216a-5p. Western blot analysis was performed to detect LC3-I, LC3-II, Beclin-1 and p62 levels. The autophagosome formation was analyzed by immunofluorescence analysis. Cell apoptosis was measured by flow cytemotry and caspase 3 activity. Dual-luciferase reporter assay or RNA immunorecipitation assay was performed to verify the targeted interrelation between MALAT1 and miR-216a-5p, or miR-216a-5p and Beclin-1. Our data revealed that MALAT1 was upregulated and miR-216a-5p was downregulated in serum of AS patients and ox-LDL-treated HUVECs. ox-LDL treatment induced HUNECs autophagy. Moreover, MALAT1 enhanced autophagy and survival in ox-LDL-treated HUVECs. MALAT1 directly binded to miR-216a-5p and MALAT1 enhanced Beclin-1 expression by sponging miR-216a-5p. Also, miR-216-5p-mediated repressive effect on autophagy and survival was abrogated by MALAT1. Additionally, Beclin-1 knockdown inhibited autophagy and survival in ox-LDL-treated HUVECs. In all, our data suggested that MALAT1 might play a protective role at least partly by sponging miR-216a-5p and regulating Beclin-1, highlighting that MALAT1 might be a potential therapeutic target of AS.