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Original Research Article | OPEN ACCESS

LINC-ROR regulates myocardial ischemia/reperfusion injury via targeting of miR-129-5p/Hook3 axis

Yan Chen1, Qianqian Guan2, Xiuyuan Feng1 , Xuejun Jiang3, Guang Xu1, Hongwei Hou1 BiKe 1

1Department of Cardiology, Ezhou Central Hospital, Ezhou; 2Department of Cardiology, Puren Hospital of Wuhan; 3Department of Cardiology, Hubei Provincial People's Hospital, Wuhan, Hubei Province 43000, China.

For correspondence:-  Xiuyuan Feng   Email: fengxiuyuan666@163.com   Tel:+862760660503

Accepted: 28 February 2021        Published: 31 March 2021

Citation: Chen Y, Guan Q, Feng X, Jiang X, Xu G, Hou H, et al. LINC-ROR regulates myocardial ischemia/reperfusion injury via targeting of miR-129-5p/Hook3 axis. Trop J Pharm Res 2021; 20(3):445-451 doi: 10.4314/tjpr.v20i3.1

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the underlying mechanism of long intergenic non-protein coding RNA (LINC-ROR) in myocardial ischemia/reperfusion (I/R) injury.
Methods: Rat H9C2 cells were used to establish the model of hypoxia/reoxygenation (H/R). Cell viability was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. The proportion of apoptotic H9C2 cells was evaluated using flow cytometry. Luciferase reporter experiments and RNA pull-down assays were used to determine the relationships among LINC-ROR, miR-129-5p, and hook microtubule tethering protein 3 (Hook3), while QRT-PCR and western blots were used to investigate the relationship between LINC-ROR and the expression and activation of Hook3 and proteins of the PI3K/AKT/mTOR pathway.

Results: LINC-ROR was elevated under H/R stimulation. The viability of H9C2 cells decreased, and cell apoptosis was induced after H/R treatment. These latter effects were abrogated by the down-regulation of LINC-ROR. Luciferase reporter results and RNA pull-down showed that LINC-ROR served as the miR-129-5p sponge, and miR-129-5p was bound to Hook3 RNA directly. Moreover, overexpression of LINC-ROR increased Hook3 protein level by serving as miR-129-5p sponge. Furthermore, the overexpression of LINC-ROR activated PI3K/Akt/mTOR pathway by regulating Hook3.

Conclusion: LINC-ROR increases in cardiomyocytes with H/R injury. Down-regulation of LINC-ROR alleviates myocardial I/R injury via miR-129-5p/Hook3 axis. Therefore, LINC-ROR is a potential therapeutic target for myocardial I/R injury.

Keywords: LINC-ROR, miR-129-5p, Hook3, Ischemia/reperfusion injury, Hypoxia/reoxygenation

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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