Abstract

Resident muscle stem cells, known as satellite cells, are thought to be hallmarks of skeletal muscle plasticity. It is generally well accepted that satellite cells are essential for muscle regeneration following injury, however, their role in muscle regrowth following an atrophic stimuli remains unclear. The current study employed a genetically modified mouse model (Pax7‐DTA) that allowed for the effective ablation of >90% of satellite cells in adulthood. Control and satellite cell ablated young female mice were either hindlimb suspended (HS) for 14 days, or HS for 14 days followed by 14 days of reloading to follow regrowth. Muscle atrophy as measured by whole muscle wet weight, fiber cross‐sectional area and single‐fiber width occurred in response to HS and did not differ between satellite cell ablated muscles and control muscles. Furthermore, the absence of satellite cells did not attenuate muscle mass recovery during the reloading period, suggesting that satellite cells are not mandatory for muscle regrowth. Interestingly, the myonuclei from satellite cell ablated muscles were longer than myonuclei from non‐ablated muscles, alluding to a potential mechanism of regulation between satellite cells and myonuclear size. The data from the present study suggest that satellite cells are not a requirement for muscle regrowth following atrophy; however, their absence may alter myonuclear size. NIAMS: R01AR060701

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