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...
Main Authors: | , , , , , , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Frontiers Media S.A.
2021-08-01
|
Series: | Frontiers in Cardiovascular Medicine |
Subjects: | |
Online Access: | https://www.frontiersin.org/articles/10.3389/fcvm.2021.654969/full |
_version_ | 1818910253444497408 |
---|---|
author | Lin Du Lin Du Jie Chen Yong Wu Guangwei Xia Mingxing Chen Pei Zhao Yao Wang Deshan Yao Fan Liu Lina Zhang Xue Wang Yi Yang Liansheng Wang |
author_facet | Lin Du Lin Du Jie Chen Yong Wu Guangwei Xia Mingxing Chen Pei Zhao Yao Wang Deshan Yao Fan Liu Lina Zhang Xue Wang Yi Yang Liansheng Wang |
author_sort | Lin Du |
collection | DOAJ |
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 H2O2 and CoCl2 treatments and N1LR overexpression alleviated apoptosis, inflammation reaction, and LDH release in cardiomyocytes treated with H2O2 and CoCl2. 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 H2O2. 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. |
first_indexed | 2024-12-19T22:39:52Z |
format | Article |
id | doaj.art-6de8c569604640b0b955806ae4f3a3c7 |
institution | Directory Open Access Journal |
issn | 2297-055X |
language | English |
last_indexed | 2024-12-19T22:39:52Z |
publishDate | 2021-08-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Cardiovascular Medicine |
spelling | doaj.art-6de8c569604640b0b955806ae4f3a3c72022-12-21T20:03:06ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2021-08-01810.3389/fcvm.2021.654969654969Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling PathwayLin Du0Lin Du1Jie Chen2Yong Wu3Guangwei Xia4Mingxing Chen5Pei Zhao6Yao Wang7Deshan Yao8Fan Liu9Lina Zhang10Xue Wang11Yi Yang12Liansheng Wang13Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Gastroenterology, Northern Jiangsu Province People's Hospital, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, ChinaDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, ChinaLong 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 H2O2 and CoCl2 treatments and N1LR overexpression alleviated apoptosis, inflammation reaction, and LDH release in cardiomyocytes treated with H2O2 and CoCl2. 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 H2O2. 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.https://www.frontiersin.org/articles/10.3389/fcvm.2021.654969/fullacute myocardial infarctionLncRNA N1LRischemic reperfusion injurycardiomyocytesTGF-β pathway |
spellingShingle | Lin Du Lin Du Jie Chen Yong Wu Guangwei Xia Mingxing Chen Pei Zhao Yao Wang Deshan Yao Fan Liu Lina Zhang Xue Wang Yi Yang Liansheng Wang Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway Frontiers in Cardiovascular Medicine acute myocardial infarction LncRNA N1LR ischemic reperfusion injury cardiomyocytes TGF-β 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 | acute myocardial infarction LncRNA N1LR ischemic reperfusion injury cardiomyocytes TGF-β pathway |
url | https://www.frontiersin.org/articles/10.3389/fcvm.2021.654969/full |
work_keys_str_mv | AT lindu longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT lindu longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT jiechen longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT yongwu longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT guangweixia longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT mingxingchen longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT peizhao longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT yaowang longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT deshanyao longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT fanliu longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT linazhang longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT xuewang longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT yiyang longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway AT lianshengwang longnoncodingrnan1lrprotectsagainstmyocardialischemicreperfusioninjurythroughregulatingthetgfbsignalingpathway |