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* To whom correspondence should be addressed. E-mail: gpavlat{at}emory.edu.
Atrophy of skeletal muscle leads to decreases in myofiber size and nuclear number, however the effects of atrophic conditions on muscle precursor cells (MPCs) are largely unknown. MPCs lie outside myofibers and represent the main source of additional myonuclei necessary for muscle growth and repair. Here, we examine the properties of MPCs after hindlimb suspension (HS)- induced atrophy and subsequent recovery of the mouse hindlimb muscles. We demonstrate that the number of MPCs in atrophied muscles is decreased. RT-PCR analyses of cells isolated from atrophied muscles indicate that several mRNAs characteristic of the myogenic program in MPCs are absent. Cells isolated from atrophied muscles fail to properly proliferate and undergo differentiation into multinucleated myotubes. Thus, atrophy leads to a decrease in MPCs and causes dysfunction in those MPCs that remain. Upon regrowth of the atrophied muscles, these deleterious effects are reversed. Our data suggest that preventing loss or dysfunction of MPCs may be a new pharmacological target during muscle atrophy.
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