Myogenin Regulates DUSP13 to Inhibit Apoptosis Induced by Reactive Oxygen Species.
apoptosis
cardiomyocyte
myogenin
p38 MAPK pathway
reactive oxygen species
Journal
Frontiers in bioscience (Landmark edition)
ISSN: 2768-6698
Titre abrégé: Front Biosci (Landmark Ed)
Pays: Singapore
ID NLM: 101612996
Informations de publication
Date de publication:
04 Feb 2024
04 Feb 2024
Historique:
received:
21
06
2023
revised:
21
11
2023
accepted:
11
12
2023
medline:
29
2
2024
pubmed:
29
2
2024
entrez:
29
2
2024
Statut:
ppublish
Résumé
Myogenin is well known as a crucial transcription factor in skeletal muscle development, yet its other biological functions remain unexplored. Previous research showed that myogenin suppresses apoptosis induced by angiotensin II in human induced pluripotent stem cell-derived cardiomyocytes, and offered a new perspective on myogenin's role in cardioprotection. However, the detailed mechanism of this cardioprotection, especially under oxidative stress, is still unclear. In this study, hydrogen peroxide (H2O2) was used to generate reactive oxygen species in myogenin-overexpressing cardiomyocytes. The apoptosis was examined by flow cytometry. Transcriptome sequencing (RNA-seq) was performed to identify genes regulated by myogenin. Western blotting was used to detect the protein level of Flow cytometry analysis of apoptosis showed that overexpressing myogenin for 24 and 48 hours decreased the apoptotic ratio by 47.9% and 63.5%, respectively, compared with untreated controls. Transcriptome sequencing performed on cardiomyocytes that expressed myogenin for different amounts of time (6, 12, 24, and 48 hours) identified The present findings suggest that myogenin might attenuate apoptosis induced by reactive oxygen species by up-regulating
Sections du résumé
BACKGROUND
BACKGROUND
Myogenin is well known as a crucial transcription factor in skeletal muscle development, yet its other biological functions remain unexplored. Previous research showed that myogenin suppresses apoptosis induced by angiotensin II in human induced pluripotent stem cell-derived cardiomyocytes, and offered a new perspective on myogenin's role in cardioprotection. However, the detailed mechanism of this cardioprotection, especially under oxidative stress, is still unclear.
METHODS
METHODS
In this study, hydrogen peroxide (H2O2) was used to generate reactive oxygen species in myogenin-overexpressing cardiomyocytes. The apoptosis was examined by flow cytometry. Transcriptome sequencing (RNA-seq) was performed to identify genes regulated by myogenin. Western blotting was used to detect the protein level of
RESULTS
RESULTS
Flow cytometry analysis of apoptosis showed that overexpressing myogenin for 24 and 48 hours decreased the apoptotic ratio by 47.9% and 63.5%, respectively, compared with untreated controls. Transcriptome sequencing performed on cardiomyocytes that expressed myogenin for different amounts of time (6, 12, 24, and 48 hours) identified
CONCLUSIONS
CONCLUSIONS
The present findings suggest that myogenin might attenuate apoptosis induced by reactive oxygen species by up-regulating
Identifiants
pubmed: 38420814
pii: S2768-6701(23)01152-8
doi: 10.31083/j.fbl2902049
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
49Subventions
Organisme : Guangdong Basic and Applied Basic Research Foundation
ID : 2021A1515111152
Organisme : National Natural Science Foundation of China
ID : U2005214
Organisme : National Key R&D Program of China
ID : 2022YFB4600600
Informations de copyright
© 2024 The Author(s). Published by IMR Press.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest. However, it should be noted that Lishi Zhou and Bin Lin are affiliated with Guangdong Beating Origin Regenerative Medicine Co., Ltd. Steps have been taken to ensure that their involvement in this research did not influence the objectivity and integrity of the study findings.