The Polycomb group gene BMI1 is essential for efficient muscle regeneration in a mouse model of Duchenne Muscular Dystrophy and its enhanced expression in adult skeletal muscle satellite cells ameliorates the muscle strength in this model. In this experiment, we investigated the impact of mild BMI1 overexpression in human cells. We showed translation between observed mouse and human phenotypes. In human myoblasts, BMI1 overexpression increases mitochondrial activity leading to an enhanced energetic state with increased ATP production and concomitant protection against DNA damage both in vitro and upon xenografting in a severe dystrophic mouse model. These preclinical data in mouse models and in human cells provide a strong rationale for the development of pharmacological approaches to target BMI1-mediated mitochondrial regulation and protection from DNA damage to sustain the regenerative potential of the skeletal muscle in conditions of chronic muscle wasting. This ArrayExpress record is for the RNA-seq data from three independently prepared normal and DMD myoblasts cell cultures infected with GFP and BMI1Over lentiviral particles and induced to differentiate for 2 days.
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