LncRNA KCNQ1OT1 Affects LPS-Induced Apoptosis and Inflammatory Response of Vascular Endothelial Cells: the Underlying Mechanism 

This study investigated whether lncRNA KCNQ1OT1 acted on LPS-induced VEC (vascular endothelial cell) apoptosis and the expression of pro-inflammatory cytokines, as well as elucidated its action mechanism. VECs were stimulated with 1.0 mg/mL LPS for 24 h following transfection of KCNQ1OT1 overexpressionvector and/or miR-223 inhibitor. The expression of KCNQ1OT1 and miR-223 was detected by RT-qPCR. Cellapoptosis was examined with flow cytometry. The protein expression of Bcl-2 and Bax was assayed by Western blot. The level of TNF-α, IL-1 and IL-6 in the supernatant was measured utilizing ELISA kit. The regulatory interaction between KCNQ1OT1 and miR-223 was verified by dual-luciferase reporter assay. The results showedLPS stimulation inhibited KCNQ1OT1 expression and promoted miR-223 expression. KCNQ1OT1 upregulationor miR-223 downregulation decreased LPS-induced VEC apoptosis and the expression of Bax, TNF-α, IL-1 andIL-6 (P<0.05), while increased that of Bcl-2 (P<0.05). KCNQ1OT1 negatively regulated miR-223 xpression, asmiR-223 upregulation reversed the inhibitory effect of KCNQ1OT1 upregulation on the apoptosis of VECs andthe inflammatory cytokine expression both induced by LPS. These results collectively suggest that KCNQ1OT1upregulation inhibits LPS-induced VEC apoptosis and inflammatory response. Its action mechanism is possible associated with the negative regulation of miR-223. The KCNQ1OT1/miR-22axis may serve as a novel target in thetreatment of vascular endothelial cell injury.