LncRNA uc003pxg.1 Interacts With miR-339-5p Promote Vascular Endothelial Cell Proliferation, Migration and Angiogenesis

Background and Objectives: This study aimed to investigate the roles of lncRNA uc003pxg.1 and miR-339-5p in regulating the occurrence and development of coronary heart disease. Methods: First, the expression levels of uc003pxg.1 and miR-339-5p were verified in peripheral blood mononuclear cells of clinical samples. Then, the target gene was identified using high-throughput sequencing combined with bioinformatics. Human umbilical vein endothelial cells (HUVECs) were transfected with si-uc003pxg.1, miR-339-5p mimic and miR339-5p inhibitor, and the expression of related genes was detected by reverse transcription-quantitative polymerase chain reaction and western blotting. EdU, CCK-8, Cell scratch and Transwell assays were used to analyze the effects of uc003pxg.1 and miR-339-5p on cell proliferation and migration. Results: The expression of uc003pxg.1 and miR-339-5p was negatively correlated in clinical samples and HUVECs. The si-uc003pxg.1 and miR-339-5p mimic decreased the proliferation and migration of HUVECs and decreased the expression of transforming growth factor (TGF)-(31 and alpha-smooth muscle actin (SMA). The protein expression levels ofTGF-(31, alpha-SMA, CD31, collagen I, collagen III and endoglin were decreased, and angiogenesis was weakened. The miR-339-5p inhibitor had the opposite effect. Conclusions: Our study revealed that upregulation of uc003pxg.1 and downregulation of miR-339-5p in vitro promote cell proliferation, cell migration and angiogenesis and upregulate the expression ofTGF-(31, alpha-SMA, CD31, collagen I, collagen III and endoglin, which may lead to the development of vascular atherosclerosis.