CTBP1‑AS2 inhibits proliferation and inducesautophagy in ox‑LDL‑stimulated vascular smooth musclecells by regulating miR‑195‑5p/ATG14.

Abstract

Atherosclerosis (AS) is a chronic progressive disease caused by injury and functional changes in vascular smooth muscle cells (VSMCs). Long non‑coding RNAs (lncRNAs) are pivotal regulators in AS development. The present study aimed to explore the roles and molecular mechanisms of lncRNA CTBP1‑AS2 in AS progression. A dual‑luciferase reporter assay confirmed that miR‑195‑5p is a downstream target miRNA of lncRNA CTBP1‑AS2 and miR‑195‑5p was increased in AS. The expression levels of miR‑195‑5p and CTBP1‑AS2 in the serums of patients with AS and human aorta vascular smooth muscle cells was increased or decreased, respectively, following treatment with oxidized low‑density lipoprotein (ox‑LDL). Functional experiments showed that the overexpression of lncRNA CTBP1‑AS2 inhibited the proliferation of HA‑VSMCs and promoted their autophagy following ox‑LDL treatment. This effect could be reversed by treatment with ROC‑325, the inhibitor of autophagy, or miR‑195‑5p mimics. Autophagy related 14 (ATG14) was identified to be a target of miR‑195‑5p, and lncRNA CTBP1‑AS2 promoted ATG14 expression by serving as a competing endogenous RNA of miR‑195‑5p. The present study revealed that lncRNA CTBP1‑AS2 may serve a role in AS by inhibiting the proliferation and promoting the autophagy of VSMCs through ATG14 modulation via miR‑195‑5p. These data may provide a novel therapeutic target for AS.