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MG149 Inhibits MOF-Mediated p53 Acetylation to Attenuate X-Ray Radiation-Induced Apoptosis in H9c2 Cells
Qianwen Nie1,2, Xuan Huan1,2, Jing Kang1,2
1Lanzhou University Second College of Clinical Medicine, Chengguan District, Lanzhou 730030, China.
Abstract:
Cardiomyocyte apoptosis is involved in the pathogenesis of radiation-induced heart disease, but the underlying epigenetic mechanism remains elusive. We evaluated the potential mediating role of males absent on the first (MOF) in the association between epigenetic activation of p53 lysine 120 (p53K120) and X-ray radiation-induced apoptosis in H9c2 cells. H9c2 cells were pretreated for 24 h with the MOF inhibitor MG149 after 4 Gy irradiation, followed by assessment of cell proliferation, injury, and apoptosis. MOF expression was upregulated by X-ray radiation. MG149 suppressed the proliferation inhibition, reduction of mitochondrial membrane potential, ROS production, and cell apoptosis. MG149 may promote the survival of H9c2 cells via inhibition of MOF-mediated p53K120 acetylation in response to X-ray radiation-induced apoptosis. Our data indicates a MOF-associated epigenetic mechanism in H9c2 cells that promotes attenuation of X-ray radiation-induced injury.
Insights
Males absent on the first (MOF) epigenetically regulates p53K120 acetylation, mediating X-ray radiation-induced cardiomyocyte apoptosis. Inhibiting MOF with MG149 protects against radiation injury by attenuating this epigenetic mechanism.
Area of Science:
- Molecular Biology
- Epigenetics
- Cardiovascular Research
Background:
- Cardiomyocyte apoptosis contributes to radiation-induced heart disease.
- The specific epigenetic mechanisms driving this process are not fully understood.
Purpose of the Study:
- To investigate the role of males absent on the first (MOF) in X-ray radiation-induced cardiomyocyte apoptosis.
- To explore the potential of MOF inhibition as a therapeutic strategy.
Main Methods:
- H9c2 cells were irradiated with 4 Gy X-rays.
- Cells were pretreated with the MOF inhibitor MG149.
- Assessed cell proliferation, injury, apoptosis, mitochondrial membrane potential, and reactive oxygen species (ROS) production.
Main Results:
- X-ray radiation upregulated MOF expression in H9c2 cells.
- MG149 treatment suppressed radiation-induced proliferation inhibition, mitochondrial dysfunction, ROS production, and apoptosis.
- MG149 inhibited MOF-mediated p53K120 acetylation.
Conclusions:
- MOF plays a mediating role in X-ray radiation-induced cardiomyocyte apoptosis via p53K120 acetylation.
- MOF inhibition presents a potential therapeutic approach to mitigate radiation-induced heart injury.
