HIX003209 promotes vascular smooth muscle cell migration and proliferation through modulating miR-6089.

Accumulating references have showed that long noncoding RNAs (lncRNAs) act important roles in the development of human diseases. The role and expression of HIX003209 remains unclear in the pathogenesis of atherosclerosis. We showed that HIX003209 expression was upregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. HIX003209 was overexpressed in vascular smooth muscle cells (VSMCs) induced by inflammatory mediators including tumor necrosis factor-α(TNF-α), ox-LDL and latelet-derived growth factor-BB (PDGF-BB). Ectopic expression of HIX003209 enhanced cell growth and migration and induced inflammatory mediators secretion such as interleukin 6 (IL-6), TNF-α and IL-1β in VSMCs. Furthermore, we showed that miR-6089 was downregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. There was a negative association between expression of HIX003209 and miR-6089 in atherosclerotic coronary tissues. MiR-6089 expression was decreased in VSMCs induced by inflammatory mediators including TNF-α, ox-LDL and PDGF-BB. Dual luciferase analysis showed that miR-6089 overexpression decreased luciferase activity of HIX003209 WT-type 3'-UTR but not the mut-type 3'-UTR. Overexpression of HIX003209 suppressed the expression of miR-6089 in VSMCs. Ectopic expression of HIX003209 induced cell growth, migration and the secretion of inflammatory mediators via regulating miR-6089 expression. These data suggested that HIX003209 promoted VSMCs proliferation, migration and the secretion of inflammatory mediators partly via regulating miR-6089.