Research Paper Volume 13, Issue 8 pp 11188—11206
Silencing long non-coding RNA MIAT ameliorates myocardial dysfunction induced by myocardial infarction via MIAT/miR-10a-5p/EGR2 axis
- 1 School of Life Sciences, North China University of Science and Technology, Tangshan 063210, P.R. China
- 2 Department of Preventive Health, The Third People’s Hospital Of Xiangcheng District In Suzhou, Suzhou 215134, P.R. China
- 3 Department of Pediatrics, North China University of Science and Technology Affiliated Hospital, Tangshan 063000, P.R. China
- 4 Department of Neurology, Tangshan Gongren Hospital, Tangshan 063000, P.R. China
- 5 Department of Cardiovascular Diseases, North China University of Science and Technology Affiliated Hospital, Tangshan 063000, P.R. China
- 6 Department of Anesthesiology, North China University of Science and Technology Affiliated Hospital, Tangshan 063000, P.R. China
- 7 Department of Neurology, Tangshan People’s Hospital, Tangshan 063001, P.R. China
Received: February 13, 2020 Accepted: October 20, 2020 Published: March 26, 2021https://doi.org/10.18632/aging.202785
How to Cite
Copyright: © 2021 Cao 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 RNA (lncRNA) myocardial infarction-associated transcript (MIAT) has been widely-demonstrated to function as diagnostic markers for acute myocardial infarction (MI). This study was designed to explore the modulatory role of MIAT and its underlying molecular mechanism in MI. Firstly, MI mouse model was developed via ligation of the descending branch of the left coronary artery, and cell model was established through exposure to hypoxic conditions. Online prediction indicated that MIAT could bind to microRNA-10a-5p (miR-10a-5p), while miR-10a-5p was highlighted to bind to early growth response gene-2 (EGR2). MIAT and EGR2 were subsequently determined to be highly-expressed, whereas miR-10a-5p was found to be poorly-expressed in cardiomyocytes exposed to hypoxia as well as in MI mice using RT-qPCR and Western blot assay. The binding relationships between MIAT and miR-10a-5p, and between miR-10a-5p and EGR2 were further confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. The results of in vitro and in vivo experimentation also suggested that overexpression of miR-10a-5p or silencing of MIAT and EGR2 reduced cardiomyocyte apoptosis and increased ATP content, thus alleviating the impairment of cardiac function following MI. In a word, inhibition of MIAT protects against cardiac dysfunction induced by MI through the crosstalk with miR-10a-5p/EGR2.