AUTHOR=Du Lin , Chen Jie , Wu Yong , Xia Guangwei , Chen Mingxing , Zhao Pei , Wang Yao , Yao Deshan , Liu Fan , Zhang Lina , Wang Xue , Yang Yi , Wang Liansheng 

TITLE=Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway

JOURNAL=Frontiers in Cardiovascular Medicine

VOLUME=8

YEAR=2021

URL=https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2021.654969

DOI=10.3389/fcvm.2021.654969

ISSN=2297-055X

ABSTRACT=<p>Long non-coding RNAs (lncRNAs) have been shown to play critical roles in various cell biological processes. However, the mechanism of lncRNAs in acute myocardial infarction (AMI) is not fully understood. Previous studies showed that lncRNA N1LR was down-regulated in ischemic cerebral stroke and its up-regulation was protective. The current study was designed to assess the protective effect of N1LR and further to explore potential mechanisms of N1LR in ischemic/reperfusion (I/R) injury after AMI. Male C57BL/6J mice and H9c2 cardiomyocytes were selected to construct <italic>in vivo</italic> and <italic>in vitro</italic> pathological models. In H9c2 cell line, N1LR expression was markedly decreased after H<sub>2</sub>O<sub>2</sub> and CoCl<sub>2</sub> treatments and N1LR overexpression alleviated apoptosis, inflammation reaction, and LDH release in cardiomyocytes treated with H<sub>2</sub>O<sub>2</sub> and CoCl<sub>2</sub>. Mouse <italic>in vivo</italic> study showed that overexpression of N1LR enhanced cardiac function and suppressed inflammatory response and fibrosis. Mechanistically, we found that the expression of transforming growth factor (TGF)-β1 and smads were significantly decreased in the N1LR overexpression group exposed to H<sub>2</sub>O<sub>2</sub>. In a summary, our study indicated that N1LR can act as a protective factor against cardiac ischemic-reperfusion injury through regulating the TGF-β/Smads signaling pathway.</p>