LncRNA A2M-AS1 lessens the injury of cardiomyocytes caused by hypoxia and reoxygenation via regulating IL1R2
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Genes & Genomics https://doi.org/10.1007/s13258-020-01007-6
RESEARCH ARTICLE
LncRNA A2M‑AS1 lessens the injury of cardiomyocytes caused by hypoxia and reoxygenation via regulating IL1R2 Xue‑Lian Song1 · Fei‑Fei Zhang2 · Wen‑Jing Wang2 · Xin‑Ning Li2 · Yi Dang2 · Ying‑Xiao Li2 · Qian Yang2 · Mei‑Jing Shi2 · Xiao‑Yong Qi1,2 Received: 5 July 2020 / Accepted: 29 September 2020 © The Genetics Society of Korea 2020
Abstract Background Myocardial ischemia and reperfusion injury (MI/RI) is a complex pathophysiological process, which can lead to severe myocardial injury. The long noncoding RNA alpha-2-macroglobulin antisense RNA 1 (A2M-AS1) has been revealed to be abnormally expressed in MI, However, its function in MI and the potential mechanism are still unclear. Objective To evaluate the functional role of A2M-AS1 in hypoxia/reoxygenation (H/R)-induced neonatal cardiomyocytes and its potential molecular mechanism. Methods Dataset GSE66360 was obtained from GEO database for analyzing the RNA expression of A2M-AS1 and interleukin 1 receptor type 2 (IL1R2). KEGG pathway enrichment analysis of the genes that co-expressed with A2M-AS1 was performed. Human neonatal cardiomyocytes were subjected to H/R to construct in vitro models. QRT-PCR and Western blot were adopted to test the levels of mRNA and protein. The viability and apoptosis of cardiomyocytes were tested by CCK-8 and flow cytometry assays, respectively. Results The expression of A2M-AS1 was notably downregulated in H/R-treated cardiomyocytes. Overexpression of A2MAS1 can notably enhance the cell viability of H/R-damaged cardiomyocytes, whereas knockdown of A2M-AS1 showed the opposite outcomes. Besides, a negative correlation was showed between A2M-AS1 and IL1R2 expression. In H/R-treated cardiomyocytes, overexpression of IL1R2 weakened the promoting proliferation and anti-apoptosis effects caused by overexpressing A2M-AS1, however, IL1R2-knockdown abolished the anti-proliferation and pro-apoptosis effects caused by silencing A2M-AS1. Conclusion This study demonstrates the potential regulatory role of A2M-AS1/ IL1R2 axis in cardiomyocytes suffered from H/R, and provides insight into the protection of MI/RI. Keywords Myocardial ischemia and reperfusion injury · Apoptosis · Proliferation · Alpha-2-macroglobulin antisense RNA 1 · Interleukin 1 receptor type 2
Introduction
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s13258-020-01007-6) contains supplementary material, which is available to authorized users. * Xiao‑Yong Qi [email protected] 1
Graduate School, Hebei Medical University, Shijiazhuang 050017, Hebei, People’s Republic of China
Department of Cardiology Center, Hebei General Hospital, No. 348 of Heping West Road, Shijiazhuang 050051, Hebei, People’s Republic of China
2
Acute myocardial infarction (AMI) refers to the myocardial necrosis and injury caused by sustainable myocardial ischemia and hypoxia (Anderson and Morrow 2017). It is a crucial cause of morbidity and mortality worldwide, a
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