lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats
ObjectiveSympathetic remodeling after myocardial infarction (MI) is the primary cause of ventricular arrhythmias (VAs), leading to sudden cardiac death (SCD). M1-type macrophages are closely associated with inflammation and sympathetic remodeling after MI. Long noncoding RNAs (lncRNAs) are critical...
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| Format: | Article |
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Frontiers Media S.A.
2023-01-01
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| Series: | Frontiers in Cardiovascular Medicine |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fcvm.2022.1019435/full |
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| author | Pingjiang Li Pingjiang Li Kang Wang Jie Yin Lei Qi Lei Qi Hesheng Hu Peijin Yang Peijin Yang Yugen Shi Yan Li Meng Feng Meng Feng Hangji Lyu Hangji Lyu Weili Ge Xiaolu Li Suhua Yan |
| author_facet | Pingjiang Li Pingjiang Li Kang Wang Jie Yin Lei Qi Lei Qi Hesheng Hu Peijin Yang Peijin Yang Yugen Shi Yan Li Meng Feng Meng Feng Hangji Lyu Hangji Lyu Weili Ge Xiaolu Li Suhua Yan |
| author_sort | Pingjiang Li |
| collection | DOAJ |
| description | ObjectiveSympathetic remodeling after myocardial infarction (MI) is the primary cause of ventricular arrhythmias (VAs), leading to sudden cardiac death (SCD). M1-type macrophages are closely associated with inflammation and sympathetic remodeling after MI. Long noncoding RNAs (lncRNAs) are critical for the regulation of cardiovascular disease development. Therefore, this study aimed to identify the lncRNAs involved in MI and reveal a possible regulatory mechanism.Methods and resultsM0- and M1-type macrophages were selected for sequencing and screened for differentially expressed lncRNAs. The data revealed that lncRNA LOC100911717 was upregulated in M1-type macrophages but not in M0-type macrophages. In addition, the lncRNA LOC100911717 was upregulated in heart tissues after MI. Furthermore, an RNA pull-down assay revealed that lncRNA LOC100911717 could interact with growth-associated protein 43 (GAP43). Essentially, immunofluorescence assays and programmed electrical stimulation demonstrated that GAP43 expression was suppressed and VA incidence was reduced after lncRNA LOC100911717 knockdown in rat hearts using an adeno-associated virus.ConclusionsWe observed a novel relationship between lncRNA LOC100911717 and GAP43. After MI, lncRNA LOC100911717 was upregulated and GAP43 expression was enhanced, thus increasing the extent of sympathetic remodeling and the frequency of VA events. Consequently, silencing lncRNA LOC100911717 could reduce sympathetic remodeling and VAs. |
| first_indexed | 2024-04-11T00:37:21Z |
| format | Article |
| id | doaj.art-c2dae8be53694785a5183082fa35e583 |
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| issn | 2297-055X |
| language | English |
| last_indexed | 2024-04-11T00:37:21Z |
| publishDate | 2023-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cardiovascular Medicine |
| spelling | doaj.art-c2dae8be53694785a5183082fa35e5832023-01-06T17:02:34ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2023-01-01910.3389/fcvm.2022.10194351019435lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in ratsPingjiang Li0Pingjiang Li1Kang Wang2Jie Yin3Lei Qi4Lei Qi5Hesheng Hu6Peijin Yang7Peijin Yang8Yugen Shi9Yan Li10Meng Feng11Meng Feng12Hangji Lyu13Hangji Lyu14Weili Ge15Xiaolu Li16Suhua Yan17Department of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, ChinaShandong First Medical University and Shandong Academy of Medical Sciences, Jinan, ChinaDepartment of Cardiology, Cheeloo College of Medicine, Shandong Qianfoshan Hospital, Shandong University, Jinan, ChinaDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, ChinaDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, ChinaShandong First Medical University and Shandong Academy of Medical Sciences, Jinan, ChinaDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, ChinaDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, ChinaShandong First Medical University and Shandong Academy of Medical Sciences, Jinan, ChinaDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, ChinaShandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Medical Research Center, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Jinan, ChinaDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, ChinaShandong First Medical University and Shandong Academy of Medical Sciences, Jinan, ChinaDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, ChinaShandong First Medical University and Shandong Academy of Medical Sciences, Jinan, ChinaDepartment of Cardiology, Taizhou Hospital, Wenzhou Medical University, Taizhou, Zhejiang, ChinaDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, ChinaDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, ChinaObjectiveSympathetic remodeling after myocardial infarction (MI) is the primary cause of ventricular arrhythmias (VAs), leading to sudden cardiac death (SCD). M1-type macrophages are closely associated with inflammation and sympathetic remodeling after MI. Long noncoding RNAs (lncRNAs) are critical for the regulation of cardiovascular disease development. Therefore, this study aimed to identify the lncRNAs involved in MI and reveal a possible regulatory mechanism.Methods and resultsM0- and M1-type macrophages were selected for sequencing and screened for differentially expressed lncRNAs. The data revealed that lncRNA LOC100911717 was upregulated in M1-type macrophages but not in M0-type macrophages. In addition, the lncRNA LOC100911717 was upregulated in heart tissues after MI. Furthermore, an RNA pull-down assay revealed that lncRNA LOC100911717 could interact with growth-associated protein 43 (GAP43). Essentially, immunofluorescence assays and programmed electrical stimulation demonstrated that GAP43 expression was suppressed and VA incidence was reduced after lncRNA LOC100911717 knockdown in rat hearts using an adeno-associated virus.ConclusionsWe observed a novel relationship between lncRNA LOC100911717 and GAP43. After MI, lncRNA LOC100911717 was upregulated and GAP43 expression was enhanced, thus increasing the extent of sympathetic remodeling and the frequency of VA events. Consequently, silencing lncRNA LOC100911717 could reduce sympathetic remodeling and VAs.https://www.frontiersin.org/articles/10.3389/fcvm.2022.1019435/fulllncRNA LOC100911717GAP43macrophagemyocardial infarctionsympathetic neural remodeling |
| spellingShingle | Pingjiang Li Pingjiang Li Kang Wang Jie Yin Lei Qi Lei Qi Hesheng Hu Peijin Yang Peijin Yang Yugen Shi Yan Li Meng Feng Meng Feng Hangji Lyu Hangji Lyu Weili Ge Xiaolu Li Suhua Yan lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats Frontiers in Cardiovascular Medicine lncRNA LOC100911717 GAP43 macrophage myocardial infarction sympathetic neural remodeling |
| title | lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats |
| title_full | lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats |
| title_fullStr | lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats |
| title_full_unstemmed | lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats |
| title_short | lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats |
| title_sort | lncrna loc100911717 targeting gap43 mediated sympathetic remodeling after myocardial infarction in rats |
| topic | lncRNA LOC100911717 GAP43 macrophage myocardial infarction sympathetic neural remodeling |
| url | https://www.frontiersin.org/articles/10.3389/fcvm.2022.1019435/full |
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