RETRACTED: LncRNA PVT1 Promotes Hypoxia-Induced Cardiomyocyte Injury by Inhibiting miR-214-3p (Retracted Article)

被引:10
|
作者
Liu, Chuanliang [1 ]
Zhang, Jieqiong [2 ]
Lun, Xuejie [3 ]
Li, Lei [2 ]
机构
[1] Weifang Peoples Hosp, Dept Hlth Care 1, Weifang, Peoples R China
[2] Weifang Peoples Hosp, Dept Hlth Care 3, 151 Guangwen St, Weifang 261041, Shandong, Peoples R China
[3] Weifang Municipal Hosp, Dept Internal Med, Weifang, Peoples R China
关键词
SMOOTH-MUSCLE; APOPTOSIS; MIR-145; ACTIVATION; PROTEIN; DAMAGE;
D O I
10.1155/2021/4604883
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
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.
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页数:9
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