LncRNA PARD3-AS1 regulates the proliferation and migration of human umbilical vein endothelial cells in atherosclerosis by targeting miR-668-3p.

Abstract

Long non-coding RNAs (lncRNAs) play crucial roles in the onset and progression of cardiovascular disease, particularly atherosclerosis. However, the role of PARD3-AS1 in atherosclerosis remains largely uncharacterized. This study therefore aimed to investigate the impact of the PARD3-AS1/miR-668-3p axis on atherosclerosis. The expression levels of PARD3-AS1 and miR-668-3p in human umbilical vein endothelial cells (HUVECs) were quantified by quantitative real-time polymerase chain reaction (RT-qPCR). HUVEC proliferation was assessed using a Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2'-deoxyuridine (EdU) incorporation, and migratory and invasive capacities were evaluated using wound healing and Transwell assays. The interaction between PARD3-AS1 and miR-668-3p was confirmed by bioinformatics analysis and dual-luciferase reporter assays. In addition, serum samples were collected from patients diagnosed with atherosclerosis, and ApoE⁻/⁻ C57BL/6 mice were fed a high-fat diet for 8 weeks to establish a model of atherosclerosis. PARD3-AS1 expression was significantly reduced in the serum of patients with atherosclerosis, whereas miR-668-3p levels were markedly elevated, and the two were negatively correlated. Subsequent experiments confirmed that miR-668-3p effectively reversed the promotion effects of PARD3-AS1 on HUVEC proliferation and migration. In vivo, histological staining showed that the PARD3-AS1 overexpression group exhibited improved endothelial repair. Collectively, these findings demonstrate that PARD3-AS1 directly interacts with miR-668-3p to modulate HUVEC proliferation, migration, and invasion, suggesting that PARD3-AS1 may serve as a potential therapeutic target for atherosclerosis.