knockdown displayed antiproliferative and proapoptotic effects through pathway in ox-LDL-treated vascular smooth muscle cells.

BACKGROUND

Long noncoding RNA (lncRNA)-mediated changes in gene expression contribute to atherosclerosis (AS) development. However, the roles of numerous lncRNAs in AS have not been fully elucidated. Here, we aimed to investigate the potential role of () in autophagy of human aortic vascular smooth muscle cells (HA-VSMCs).

METHODS

expression in patients with AS was extracted from the Gene Expression Omnibus (GEO) database. and microRNA-188-3p () expression was analyzed in 20 enrolled patients with AS. HA-VSMCs were treated with oxidized low-density lipoprotein (ox-LDL) (25, 50, 75, and 100 µg/mL) for 24 h. Loss- or gain-of-function of , miR-1883p, and autophagy-related 7 () was studied using the transfected HA-VSMCs. Cell viability was assessed using Cell Counting Kit-8 (CCK-8). Apoptosis was detected with annexin V-fluorescein isothiocyanate (FITC) and propidium iodide (PI). Relative luciferase reporter assay was used to confirm the targeting relationship of to or . Gene expression was detected by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot.

RESULTS

was enriched in the serum of patients with AS and ox-LDL-treated HA-VSMCs. Ox-LDL induced proliferation and autophagy while inhibiting the apoptosis of HA-VSMCs, which was abated by knockdown. downregulated of ox-LDL-treated HA-VSMCs. knockdown caused an increase in , which inhibited proliferation and autophagy and induced the apoptosis of ox-LDL-treated HA-VSMCs. inhibited expression in ox-LDL-treated HA-VSMCs. elevated and induced autophagy through sponging in ox-LDL-treated HA-VSMCs.

CONCLUSIONS

regulated autophagy by targeting , a messenger RNA-binding miRNA that increases level, which may be a new target molecule for the prevention and prognosis of AS.