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Updated: Jul 13, 2025
A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
MG53 alleviates hypoxia/reoxygenation-induced cardiomyocyte injury by succinylation and ubiquitination modification
Yan Wang1, Hongying Zhou2, Jin Wu1
1Department of Medical Oncology, The First People's Hospital of Chun'an County(Chun'an branch of Zhejiang Provincial People's Hospital), Hangzhou, Zhejiang, China.
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.
Insights
Mitsugumin 53 (MG53) protects against heart attack by reducing cardiomyocyte injury. Its succinylation, regulated by SIRT7 and KAT3B, impacts protein levels and cell survival.
Area of Science:
- Biochemistry
- Cardiovascular Biology
- Molecular Medicine
Background:
- Mitsugumin 53 (MG53) is a key membrane repair protein implicated in acute myocardial infarction.
- Understanding MG53's role in cardiomyocyte injury is crucial for developing cardiac therapies.
Purpose of the Study:
- To investigate the impact of MG53 on cardiomyocyte injury.
- To explore the posttranslational modifications of MG53, specifically succinylation and ubiquitination.
Main Methods:
- Cardiomyocyte injury assessed via ELISA and flow cytometry.
- MG53 succinylation and ubiquitination analyzed using immunoprecipitation and western blotting.
- Interactions between MG53, KAT3B, and SIRT7 examined through co-immunoprecipitation and immunofluorescence.
Main Results:
- Overexpression of MG53 reduced hypoxia/reoxygenation-induced inflammation and apoptosis in cardiomyocytes.
- MG53 succinylation and protein levels decreased under hypoxia/reoxygenation.
- SIRT7 inhibited MG53 succinylation, while KAT3B promoted it, affecting MG53 ubiquitination and stability.
Conclusions:
- SIRT7 and KAT3B modulate MG53 succinylation at K130, influencing its ubiquitination and protein levels.
- MG53's protective effects against cardiomyocyte injury are linked to its posttranslational modifications.
- MG53 presents a potential therapeutic target for myocardial infarction treatment.
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