Abstract

Objective To explore the effect and related mechanism of LncRNA PVT1 on hypoxia-induced cardiomyocyte injury. Methods PVT1RNA and miR-214-3p levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell vitality and apoptosis were, respectively, evaluated by Cell Counting Kit-8 (CCK-8) and flow cytometry analysis. Starbase and Dual luciferase reporter (DLR) gene assay was employed to validate the interaction between miR-214-3p and PVT1. Results PVT1 was statistically upregulated, and miR-214-3p was statistically downregulated in hypoxia-induced H9c2 cells. The survival rate of H9c2 cells induced by hypoxia decreased statistically, while the apoptosis rate increased statistically (P < 0.05). PVT1 knockdown upregulated the hypoxia-induced H9c2 cell viability and inhibited apoptosis. DLR assay verified the targeting relationship between PVT1 and miR-214-3p. In addition, miR-214-3p inhibitors reversed the viability of H9c2 cells with PVT1 knockout and promoted apoptosis. Conclusion Silencing PVT1 can enhance the hypoxia-induced H9c2 cell viability and inhibit apoptosis, providing a potential target for the treatment of cardiovascular diseases.

Highlights

  • As a common disease, the incidence of cardiovascular diseases (CVDs) keeps increasing as the social environment and living habits change, which hazards human life safety [1, 2]

  • When we established a model of H9c2 cell injury using hypoxia induction, PVT1 was found to be enhanced, and miR-214-3p was statistically declined in H9c2

  • The survival rate of H9c2 cells was statistically reduced, and the apoptosis rate was statistically increased after hypoxia compared with control group

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Summary

Introduction

The incidence of cardiovascular diseases (CVDs) keeps increasing as the social environment and living habits change, which hazards human life safety [1, 2]. While for CVDs, it is of the essence to explore the mechanism of its occurrence and development and to find effective therapeutic drugs or targets. In CVDs, cardiomyocyte injury is among the key factors leading to the occurrence and development of the disease [4]. LncRNA, as a noncoding long strand RNA, plays a biological role in cells mainly through regulating protein transcription and has been found to be essential in a wide spectrum of diseases in recent years, including CVDs [7]. LncRNA PVT1 is an oncogene that exerts marked effects on multiple tumors, and studies in recent years have found that it plays a key role in some CVDs [9, 10]. Up to now, the mechanism of PVT1 in cardiomyocyte injury remains poorly understood

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