Research Paper Volume 13, Issue 10 pp 14219—14233
LncRNA AK020546 protects against cardiac ischemia–reperfusion injury by sponging miR-350-3p
- 1 Department of Intensive Care Unit, Hangzhou Hospital of Traditional Chinese Medicine (Dingqiao), Guangxing Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China
- 2 Department of Emergency Medicine, Zhejiang Provincial Peoples Hospital, People’s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China
Received: February 1, 2020 Accepted: February 25, 2021 Published: May 13, 2021https://doi.org/10.18632/aging.203038
How to Cite
Copyright: © 2021 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Long non-coding RNAs (lncRNAs) have been implicated in the development of cardiovascular diseases. We observed that lncRNA AK020546 was downregulated following ischemia/reperfusion injury to the myocardium and following H2O2 treatment in H9c2 cardiomyocytes. In vivo and in vitro studies showed that AK020546 overexpression attenuated the size of the ischemic area, reduced apoptosis among H9c2 cardiomyocytes, and suppressed the release of reactive oxygen species, lactic acid dehydrogenase, and malondialdehyde. AK020546 served as a competing endogenous RNA for miR-350-3p and activated the miR-350-3p target gene ErbB3. MiR-350-3p overexpression reversed the effects of AK020546 on oxidative stress injury and apoptosis in H9c2 cardiomyocytes. Moreover, ErbB3 knockdown alleviated the effects of AK020546 on the expression of ErbB3, Bcl-2, phosphorylated AKT, cleaved Caspase 3, and phosphorylated Bad. These findings suggest lncRNA AK020546 protects against ischemia/reperfusion and oxidative stress injury by sequestering miR-350-3p and activating ErbB3, which highlights its potential as a therapeutic target for ischemic heart diseases.