LncRNA TUG1 silencing enhances proliferation and migration of ox-LDL-treated human umbilical vein endothelial cells and promotes atherosclerotic vascular injury repairing via the Runx2/ANPEP axis.

The role of vascular endothelial cell injury in the course of atherosclerosis (AS) has attracted increasing attention. Long non-coding RNAs (LncRNAs) are demonstrated to be the biomarker for the diagnosis of AS. This study investigated the mechanism of lncRNA taurine upregulated gene 1 (TUG1) in AS. Microarray data of AS obtained from GEO database showed that lncRNA TUG1 was differentially expressed in AS samples. TUG1 expression was upregulated in ox-LDL-treated human umbilical vein endothelial cells (HUVECs). Oxidized low density lipoprotein (ox-LDL)-treated HUVECs were then transfected with sh-TUG1. TUG1 silencing promoted proliferation and migration of ox-LDL-treated HUVECs. TUG1 bound to Runt-related transcription factor 2 (Runx2). Runx2 silencing promoted proliferation and migration of HUVECs. The downstream genes of Runx2 were predicted by hTFtarget database. The binding site of Runx2 and Aminopeptidase N (ANPEP) was determined. Runx2 silencing reversed the repression effect of overexpressing ANPEP on cell proliferation and migration. TUG1 silencing inhibited ANPEP expression via Runx2 to promote HUVEC proliferation and migration. A mouse model of AS was established. The area of atherosclerotic lesions of mouse aorta was detected, and vascular re-endothelialization was evaluated. TUG1 silencing promoted vascular injury repairing and inhibited AS in vivo. In conclusion, TUG1 silencing enhanced proliferation and migration of ox-LDL-treated HUVECs and promoted vascular injury repairing in vivo via the Runx2/ANPEP axis.