MG53 alleviates hypoxia/reoxygenation-induced cardiomyocyte injury by succinylation and ubiquitination modification
Background Mitsugumin 53 (MG53) is a membrane repair factor that is associated with acute myocardial infarction. This study aimed to investigate the effects of MG53 on cardiomyocyte injury and the posttranslational modification of MG53. Methods Cardiomyocyte injury was evaluated by enzyme-linked imm...
Main Authors: | , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Taylor & Francis Group
2023-12-01
|
Series: | Clinical and Experimental Hypertension |
Subjects: | |
Online Access: | http://dx.doi.org/10.1080/10641963.2023.2271196 |
_version_ | 1827767375439593472 |
---|---|
author | Yan Wang Hongying Zhou Jin Wu Shanshan Ye |
author_facet | Yan Wang Hongying Zhou Jin Wu Shanshan Ye |
author_sort | Yan Wang |
collection | DOAJ |
description | Background Mitsugumin 53 (MG53) is a membrane repair factor that is associated with acute myocardial infarction. This study aimed to investigate the effects of MG53 on cardiomyocyte injury and the posttranslational modification of MG53. Methods Cardiomyocyte injury was evaluated by enzyme-linked immunosorbent assay and flow cytometry. The succinylation and ubiquitination levels of MG53 were examined by immunoprecipitation (IP) and western blot. The relationship between MG53 and KAT3B or SIRT7 was assessed by co-IP and immunofluorescence. Results The results showed that overexpression of MG53 inhibited inflammation response and apoptosis of cardiomyocytes induced by hypoxia/reoxygenation (H/R). Succinylation and protein levels of MG53 were downregulated in H/R-induced cells, which was inhibited by SIRT7 and promoted by KAT3B. SIRT7 aggravated and KAT3B alleviated MG53-mediated cardiomyocyte injury. Moreover, MG53 was succinylated and ubiquitinated at K130. Conclusion SIRT7 inhibited/KAT3B promoted succinylation of MG53 at K130 sites, which suppressed ubiquitination of MG53 and upregulated its protein levels, thereby alleviating H/R-induced cardiomyocyte injury. The findings suggested that MG53 may be a potential therapy for myocardial infarction. |
first_indexed | 2024-03-11T11:57:51Z |
format | Article |
id | doaj.art-81a39e6ab473422f97f92f91b4024b8f |
institution | Directory Open Access Journal |
issn | 1064-1963 1525-6006 |
language | English |
last_indexed | 2024-03-11T11:57:51Z |
publishDate | 2023-12-01 |
publisher | Taylor & Francis Group |
record_format | Article |
series | Clinical and Experimental Hypertension |
spelling | doaj.art-81a39e6ab473422f97f92f91b4024b8f2023-11-08T11:49:23ZengTaylor & Francis GroupClinical and Experimental Hypertension1064-19631525-60062023-12-0145110.1080/10641963.2023.22711962271196MG53 alleviates hypoxia/reoxygenation-induced cardiomyocyte injury by succinylation and ubiquitination modificationYan Wang0Hongying Zhou1Jin Wu2Shanshan Ye3The First People’s Hospital of Chun’an County(Chun’an branch of Zhejiang Provincial People’s Hospital)Zhejiang Provincial People’s HospitalThe First People’s Hospital of Chun’an County(Chun’an branch of Zhejiang Provincial People’s Hospital)Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical UniversityBackground Mitsugumin 53 (MG53) is a membrane repair factor that is associated with acute myocardial infarction. This study aimed to investigate the effects of MG53 on cardiomyocyte injury and the posttranslational modification of MG53. Methods Cardiomyocyte injury was evaluated by enzyme-linked immunosorbent assay and flow cytometry. The succinylation and ubiquitination levels of MG53 were examined by immunoprecipitation (IP) and western blot. The relationship between MG53 and KAT3B or SIRT7 was assessed by co-IP and immunofluorescence. Results The results showed that overexpression of MG53 inhibited inflammation response and apoptosis of cardiomyocytes induced by hypoxia/reoxygenation (H/R). Succinylation and protein levels of MG53 were downregulated in H/R-induced cells, which was inhibited by SIRT7 and promoted by KAT3B. SIRT7 aggravated and KAT3B alleviated MG53-mediated cardiomyocyte injury. Moreover, MG53 was succinylated and ubiquitinated at K130. Conclusion SIRT7 inhibited/KAT3B promoted succinylation of MG53 at K130 sites, which suppressed ubiquitination of MG53 and upregulated its protein levels, thereby alleviating H/R-induced cardiomyocyte injury. The findings suggested that MG53 may be a potential therapy for myocardial infarction.http://dx.doi.org/10.1080/10641963.2023.2271196mg53succinylationkat3bsirt7ubiquitinationhypoxia/reoxygenation |
spellingShingle | Yan Wang Hongying Zhou Jin Wu Shanshan Ye MG53 alleviates hypoxia/reoxygenation-induced cardiomyocyte injury by succinylation and ubiquitination modification Clinical and Experimental Hypertension mg53 succinylation kat3b sirt7 ubiquitination hypoxia/reoxygenation |
title | MG53 alleviates hypoxia/reoxygenation-induced cardiomyocyte injury by succinylation and ubiquitination modification |
title_full | MG53 alleviates hypoxia/reoxygenation-induced cardiomyocyte injury by succinylation and ubiquitination modification |
title_fullStr | MG53 alleviates hypoxia/reoxygenation-induced cardiomyocyte injury by succinylation and ubiquitination modification |
title_full_unstemmed | MG53 alleviates hypoxia/reoxygenation-induced cardiomyocyte injury by succinylation and ubiquitination modification |
title_short | MG53 alleviates hypoxia/reoxygenation-induced cardiomyocyte injury by succinylation and ubiquitination modification |
title_sort | mg53 alleviates hypoxia reoxygenation induced cardiomyocyte injury by succinylation and ubiquitination modification |
topic | mg53 succinylation kat3b sirt7 ubiquitination hypoxia/reoxygenation |
url | http://dx.doi.org/10.1080/10641963.2023.2271196 |
work_keys_str_mv | AT yanwang mg53alleviateshypoxiareoxygenationinducedcardiomyocyteinjurybysuccinylationandubiquitinationmodification AT hongyingzhou mg53alleviateshypoxiareoxygenationinducedcardiomyocyteinjurybysuccinylationandubiquitinationmodification AT jinwu mg53alleviateshypoxiareoxygenationinducedcardiomyocyteinjurybysuccinylationandubiquitinationmodification AT shanshanye mg53alleviateshypoxiareoxygenationinducedcardiomyocyteinjurybysuccinylationandubiquitinationmodification |