LncRNA PVT1 inhibits endothelial cells apoptosis in coronary heart disease through regulating MAPK1 expression via miR-532-3p

• Published in: Acta Cardiologica 2024-05, Vol.ahead-of-print (ahead-of-print), p.1-9
• Main Authors: Liu, Huan, Ma, Xiao-Feng, Dong, Na, Wang, Guang-Neng, Qi, Ming-Xu, Tan, Jian-Kai
• Format: Article
• Language: English
• Subjects: Apoptosis; Cell Movement; Cell Proliferation; Cells, Cultured; Coronary Artery Disease - genetics; Coronary Artery Disease - metabolism; Coronary Artery Disease - pathology; Coronary heart disease; Coronary Vessels - cytology; Coronary Vessels - pathology; Endothelial Cells - metabolism; Gene Expression Regulation - genetics; Humans; LncRNA PVT1; MicroRNAs - genetics; MicroRNAs - metabolism; migration; Mitogen-Activated Protein Kinase 1 - genetics; Mitogen-Activated Protein Kinase 1 - metabolism; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism
• ISSN: 0001-5385; 1784-973X; 0373-7934; 1784-973X
• DOI: 10.1080/00015385.2023.2209448

Background: Coronary atherosclerotic heart disease (CAD) is an inflammatory vascular disease caused by atherosclerosis. Long non-coding RNAs are involved in the pathophysiological process of coronary heart disease. Here we investigated the regulatory effects of lncRNA PVT1 (PVT1) in human coronary artery endothelial cells (HCAECs). Methods: qRT-PCR and western blot were performed to detect gene and protein expressions. CCK-8, flow cytometry and wound healing assays were used to determine cell viability, apoptosis and migration of HCAECs. The binding relationship among miR-532-3p, PVT1 and MAPK1 was verified by dual luciferase reporter assay. Results: Overexpression of PVT1 markedly reduced cell apoptosis and increased cell proliferation and migration. However, miR-532-3p upregulation suppressed cell proliferation and migration and promoted apoptosis of HCAECs. PVT1 suppressed the expression of miR-532-3p via directly targeting miR-532-3p. And miR-532-3p overexpression abolished the effect of PVT1 upregulation on proliferation and apoptosis in HCAECs. Furthermore, MAPK1 acted as a target gene of miR-532-3p and miR-532-3p inhibited MAPK1 expression. Conclusion: PVT1 promoted MAPK1 expression by targeting miR-532-3p, thus inhibiting HCAECs apoptosis and promoting cell proliferation, suggesting PVT1 might have great potential as a therapeutic target for CAD.