The long noncoding RNA uc003pxg.1 interacts with miR-339-5p to promote TGF-β1 expression and vascular endothelial cell proliferation, migration and angiogenesis in coronary heart disease

Abstract This study aims to investigate the roles of lncRNA uc003pxg.1 and miR-339-5p in regulating the proliferation, migration and angiogenesis of vascular endothelial cells and affect the occurrence and development of coronary heart disease (CHD). First, the expression levels of uc003pxg.1 and miR-339-5p were verified in clinical samples, and the correlation between them was analyzed. 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 miR-339-5p inhibitor, and the expression of related genes was detected by RT-qPCR. EdU, CCK8 and Transwell assays were used to analyze the effects of uc003pxg.1 and miR-339-5p on cell proliferation and migration. The protein expression levels were detected by western blotting and angiogenesis was observed. The expression of uc003pxg.1 and miR-339-5p was negatively correlated in clinical samples and HUVECs. si-uc003pxg.1 and miR-339-5p mimic decreased the proliferation and migration of HUVECs and decreased the expression of TGF-β1 and α-SMA. The protein expression levels of TGF-β1, α-SMA, CD31, collage I, collage III and endoglin were decreased, and angiogenesis was weakened. The miR-339-5p inhibitor had the opposite effect. Our study revealed that upregulation of uc003pxg.1 and downregulation of miR-339-5p in vivo promotes cell proliferation, cell migration and angiogenesis, and up-regulates the expression of TGF-β1, α-SMA, CD31, collage I, collage III and endoglin, which may lead to the development of vascular atherosclerosis.