Eur Rev Med Pharmacol Sci 2020; 24 (12): 6980-6993
DOI: 10.26355/eurrev_202006_21690

Hsa-circ-0068566 inhibited the development of myocardial ischemia reperfusion injury by regulating hsa-miR-6322/PARP2 signal pathway

H.-F. Zhou, L.-L. Xu, B. Xie, H.-G. Ding, F. Fang, Q. Fang

Intensive Care Unit, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou City, Zhejiang Province, PR. China. 1183005@zju.edu.cn


OBJECTIVE: In recent years, studies have shown that noncoding RNA (circRNA) is an important regulatory molecule involved in cell physiology and pathology. Herein, we analyzed the role of circRNA-68566 in the regulation of myocardial ischemia-reperfusion (I/R) injury by regulating miR-6322/PARP2 signaling pathway.

MATERIALS AND METHODS: Cell viability was checked by CCK-8; LDH concentration, ROS production, MDA, SOD and GSH-Px were measured by corresponding kits; QPCR was used to inspect the expression of circRNA-0068566 and miR-6322 in I/R injury and H9C2 cells; luciferase reporter assay confirmed the direct target effect of circRNA-0068566 and miR-6322; Western blot was used to investigate PARP2 protein expression in I/R injury and H9C2 cells.

RESULTS: We analyzed the regulatory effect of circRNA-68566 on I/R injury and found that circRNA-68566 promoted the proliferation of injured cardiomyocytes in vitro and in vivo. circRNA-68566 and miR-6322 were directly combined to regulate the development of I/R injury. We also confirmed that PARP2 was the target of miR-6322 in I/R injury.

CONCLUSIONS: We believed that circRNA-68566 participated in myocardial ischemia-reperfusion injury by regulating miR-6322/PARP2 signaling pathway, which provided a new possible strategy for the treatment of I/R injury.

Free PDF Download

To cite this article

H.-F. Zhou, L.-L. Xu, B. Xie, H.-G. Ding, F. Fang, Q. Fang
Hsa-circ-0068566 inhibited the development of myocardial ischemia reperfusion injury by regulating hsa-miR-6322/PARP2 signal pathway

Eur Rev Med Pharmacol Sci
Year: 2020
Vol. 24 - N. 12
Pages: 6980-6993
DOI: 10.26355/eurrev_202006_21690