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Am J Physiol Cell Physiol 287: C1753-C1762, 2004. First published August 25, 2004; doi:10.1152/ajpcell.00292.2004
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MUSCLE CELL BIOLOGY AND CELL MOTILITY

Skeletal muscle atrophy leads to loss and dysfunction of muscle precursor cells

Patrick O. Mitchell1,2 and Grace K. Pavlath1

1Department of Pharmacology and 2Graduate Program in Biochemistry, Cell and Developmental Biology, Emory University, Atlanta, Georgia 30322

Submitted 22 June 2004 ; accepted in final form 20 August 2004

Atrophy of skeletal muscle leads to decreases in myofiber size and nuclear number; however, the effects of atrophic conditions on muscle precursor cells (MPC) are largely unknown. MPC lie outside myofibers and represent the main source of additional myonuclei necessary for muscle growth and repair. In the present study, we examined the properties of MPC after hindlimb suspension (HS)-induced atrophy and subsequent recovery of the mouse hindlimb muscles. We demonstrated that the number of MPC in atrophied muscles was decreased. RT-PCR analysis of cells isolated from atrophied muscles indicated that several mRNA characteristic of the myogenic program in MPC were absent. Cells isolated from atrophied muscles failed to properly proliferate and undergo differentiation into multinucleated myotubes. Thus atrophy led to a decrease in MPC and caused dysfunction in those MPC that remained. Upon regrowth of the atrophied muscles, these deleterious effects were reversed. Our data suggest that preventing loss or dysfunction of MPC may be a new pharmacological target during muscle atrophy.

satellite cells; hindlimb suspension; proliferation; differentiation; myotubes


Address for reprint requests and other correspondence: G. K. Pavlath, Dept. of Pharmacology, Emory Univ. School of Medicine, 5024 O. W. Rollins Research Center, Atlanta, GA 30322 (E-mail: gpavlat{at}emory.edu)




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