LncRNA PVT1 Promotes Hypoxia-Induced Cardiomyocyte Injury by Inhibiting miR-214-3p

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.

Abnormal expression and role of MicroRNA‐214‐3p/SLC8A1 in neonatal Hypoxic‐Ischaemic encephalopathy

“…MiR‐214‐3p is also closely related to tissue hypoxic‐ischaemic injury. Studies have shown that miR‐214‐3p levels significantly decreased in hypoxia‐induced cardiomyocyte injury, and PVT1 sponged miR‐214‐3p to regulate hypoxia‐induced cardiomyocyte injury 37 . In addition, miR‐214‐3p regulates hypoxia‐mediated proliferation and pulmonary artery smooth muscle cell migration by targeting ARHGEF12 38 .…”

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