Long noncoding RNA MALAT1 promotes high glucose-induced inflammation and apoptosis of vascular endothelial cells by regulating miR-361-3p/SOCS3 axis.

Vascular complications are the important pathophysiologic manifestations of patients with diabetes mellitus (DM) and many long non-coding RNAs (LncRNAs) are involved in this process. In this study, we aimed to investigate the relationships among LncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), microRNA-361-3p (miR-361-3p), and suppressor of cytokine signaling 3 (SOCS3) in high glucose (HG)-induced human umbilical vein endothelial cell (HUVEC) injury and its underlying mechanism. We found that HG treatment significantly promotes MALAT1 and SOCS3 expressions, but inhibits miR-361-3p expression in HUVECs. Furthermore, through bioinformatics analysis and dual luciferase assay, we found that MALAT1 directly sponges miR-361-3p to counteract its suppression on SOCS3 expression. Moreover, knockdown of MALAT1 evidently inhibits HG-induced inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 expressions in HUVECs (and HUVEC apoptosis) by regulating the miR-361-3p/SOCS3 axis. In conclusion, our results indicate that knockdown of MALAT1 inhibits HG-induced vascular endothelial injury through regulating miR-361-3p/SOCS3 axis, suggesting that inhibition of MALAT1 as a potential target for endothelial injury therapy for DM.