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LncRNA A2M-AS1 lessens the injury of cardiomyocytes caused by hypoxia and reoxygenation via regulating IL1R2

Genes & Genomics 2020년 42권 12호 p.1431 ~ 1441
Song Xue-Lian, Zhang Fei-Fei, Wang Wen-Jing, Li Xin-Ning, Dang Yi, Li Ying-Xiao, Yang Qian, Shi Mei-Jing, Qi Xiao-Yong,
소속 상세정보
 ( Song Xue-Lian ) - Hebei Medical University Graduate School
 ( Zhang Fei-Fei ) - Hebei General Hospital Department of Cardiology
 ( Wang Wen-Jing ) - Hebei General Hospital Department of Cardiology
 ( Li Xin-Ning ) - Hebei General Hospital Department of Cardiology
 ( Dang Yi ) - Hebei General Hospital Department of Cardiology
 ( Li Ying-Xiao ) - Hebei General Hospital Department of Cardiology
 ( Yang Qian ) - Hebei General Hospital Department of Cardiology
 ( Shi Mei-Jing ) - Hebei General Hospital Department of Cardiology
 ( Qi Xiao-Yong ) - Hebei Medical University Graduate School

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 A2M-AS1 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.

키워드

Myocardial ischemia and reperfusion injury; Apoptosis; Proliferation; Alpha-2-macroglobulin antisense RNA 1; Interleukin 1 receptor type 2

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