Affordable Access

deepdyve-link
Publisher Website

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

Authors
  • Song, Xue-Lian1
  • Zhang, Fei-Fei2
  • Wang, Wen-Jing2
  • Li, Xin-Ning2
  • Dang, Yi2
  • Li, Ying-Xiao2
  • Yang, Qian2
  • Shi, Mei-Jing2
  • Qi, Xiao-Yong3, 4
  • 1 Graduate School, Hebei Medical University, Shijiazhuang, 050017, Hebei, People's Republic of China. , (China)
  • 2 Department of Cardiology Center, Hebei General Hospital, No. 348 of Heping West Road, Shijiazhuang, 050051, Hebei, People's Republic of China. , (China)
  • 3 Graduate School, Hebei Medical University, Shijiazhuang, 050017, Hebei, People's Republic of China. [email protected] , (China)
  • 4 Department of Cardiology Center, Hebei General Hospital, No. 348 of Heping West Road, Shijiazhuang, 050051, Hebei, People's Republic of China. [email protected] , (China)
Type
Published Article
Journal
Genes & genomics
Publication Date
Oct 14, 2020
Identifiers
DOI: 10.1007/s13258-020-01007-6
PMID: 33057899
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

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. To evaluate the functional role of A2M-AS1 in hypoxia/reoxygenation (H/R)-induced neonatal cardiomyocytes and its potential molecular mechanism. 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. 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. 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.

Report this publication

Statistics

Seen <100 times