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

Abstract

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.

Keywords:

• Coronary heart disease
• apoptosis
• migration
• LncRNA PVT1

Acknowledgements

We would like to give our sincere gratitude to the reviewers for their constructive comments.

Ethics approval and Patient consent

Serum samples were collected from 23 CAD patients and 23 healthy subjects undergoing physical examinations in the outpatient department of The Affiliated Hospital, Hengyang Medical School, University of South China. This study was passed review by Ethics Committee of the Affiliated Hospital, Hengyang Medical School, University of South China before enrolment of patients and all participants signed informed consent.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by Hunan Natural Science Foundation in 2021 (2021JJ70045) and Key Guiding Subjects of Hunan Health Commission in 2020 (No.20201905).