Knockdown of long non-coding RNA PVT1 protects human AC16 cardiomyocytes from hypoxia/reoxygenation-induced apoptosis and autophagy by regulating miR-186/Beclin-1 axis

• Published in: Gene Vol. 754; p. 144775
• Main Authors: Ouyang, Mao, Lu, Junya, Ding, Qi, Qin, Tao, Peng, Caixia, Guo, Qin
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 05.09.2020
• Subjects: Autophagy; Long non-coding RNA PVT1; microRNA-186; Myocardial ischemia/reperfusion injury; lncRNAs; ceRNAs; Long non-coding RNA PVT1; PVT1; microRNA-186; H/R; I/R; AMI; Autophagy; Myocardial ischemia/reperfusion injury; myocardial ischemia/reperfusion injury; autophagy; long non-coding RNA PVT1
• ISSN: 0378-1119; 1879-0038
• DOI: 10.1016/j.gene.2020.144775

Myocardial ischemia/reperfusion (I/R) injury is a common consequence of restored blood supply after acute myocardial infarction (AMI), but its underlying mechanisms remain largely elusive. In this study, we aimed to investigate the functional role of long non-coding RNA PVT1 in hypoxia/reoxygenation (H/R)-treated AC16 cardiomyocytes. Our experimental results demonstrated that H/R treatment impaired the viability and increased the apoptosis of AC16 cells, and knockdown of PVT1 blocked the H/R injury. Besides, PVT1 knockdown also reduced excessive autophagy in H/R-treated AC16 cells. Furthermore, we confirmed that PVT1 might serve as a ceRNA for miR-186 in AC16 cells, and rescue experiments showed that miR-186 inhibition blocked the effects of PVT1 knockdown in H/R-treated AC16 cells. In summary, this study implied that PVT1 might be a promising therapeutic target for treating myocardial I/R injury.