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

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...

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Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8414635/
https://www.ncbi.nlm.nih.gov/pubmed/34485393
http://dx.doi.org/10.3389/fcvm.2021.654969
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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
author_facet 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
author_sort Du, Lin
collection PubMed
description 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 in vivo and in vitro pathological models. In H9c2 cell line, N1LR expression was markedly decreased after H(2)O(2) and CoCl(2) treatments and N1LR overexpression alleviated apoptosis, inflammation reaction, and LDH release in cardiomyocytes treated with H(2)O(2) and CoCl(2). Mouse in vivo 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(2)O(2). 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.
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spelling pubmed-84146352021-09-04 Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway 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 Front Cardiovasc Med Cardiovascular Medicine 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 in vivo and in vitro pathological models. In H9c2 cell line, N1LR expression was markedly decreased after H(2)O(2) and CoCl(2) treatments and N1LR overexpression alleviated apoptosis, inflammation reaction, and LDH release in cardiomyocytes treated with H(2)O(2) and CoCl(2). Mouse in vivo 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(2)O(2). 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. Frontiers Media S.A. 2021-08-13 /pmc/articles/PMC8414635/ /pubmed/34485393 http://dx.doi.org/10.3389/fcvm.2021.654969 Text en Copyright © 2021 Du, Chen, Wu, Xia, Chen, Zhao, Wang, Yao, Liu, Zhang, Wang, Yang and Wang. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cardiovascular Medicine
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
Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway
title Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway
title_full Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway
title_fullStr Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway
title_full_unstemmed Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway
title_short Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway
title_sort long non-coding rna n1lr protects against myocardial ischemic/reperfusion injury through regulating the tgf-β signaling pathway
topic Cardiovascular Medicine
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8414635/
https://www.ncbi.nlm.nih.gov/pubmed/34485393
http://dx.doi.org/10.3389/fcvm.2021.654969
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