Document Detail

Skeletal muscle atrophy leads to loss and dysfunction of muscle precursor cells.
MedLine Citation:
PMID:  15329339     Owner:  NLM     Status:  MEDLINE    
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.
Patrick O Mitchell; Grace K Pavlath
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2004-08-25
Journal Detail:
Title:  American journal of physiology. Cell physiology     Volume:  287     ISSN:  0363-6143     ISO Abbreviation:  Am. J. Physiol., Cell Physiol.     Publication Date:  2004 Dec 
Date Detail:
Created Date:  2004-11-04     Completed Date:  2004-12-14     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  100901225     Medline TA:  Am J Physiol Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  C1753-62     Citation Subset:  IM    
Department of Pharmacology, Emory University School of Medicine, 5024 O. W. Rollins Research Center, Atlanta, GA 30322, USA.
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MeSH Terms
Cell Differentiation
Cell Division
Gene Expression
Hindlimb Suspension
Mice, Inbred BALB C
Mice, Inbred C57BL
Muscle Fibers, Skeletal / pathology
Muscle Proteins / genetics
Muscle, Skeletal / pathology*,  physiopathology*
Muscular Atrophy / pathology*,  physiopathology*
RNA, Messenger / analysis
Satellite Cells, Skeletal Muscle / pathology
Stem Cells / pathology*
Grant Support
Reg. No./Substance:
0/Muscle Proteins; 0/RNA, Messenger

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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