Document Detail


Damage to developing mouse skeletal muscle myotubes in culture: protective effect of heat shock proteins.
MedLine Citation:
PMID:  12598587     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Damage to skeletal muscle occurs following excessive exercise, upon reperfusion following ischaemia and in disease states, such as muscular dystrophy. Key mechanisms by which damage is thought to occur include a loss of intracellular calcium homeostasis, loss of energy supply to the cell, increased activity of oxidising free radical-mediated reactions and activation of apoptosis pathways. An increased cellular content of heat shock proteins (HSPs) has been shown to protect skeletal muscle against some forms of damage, although the mechanistic basis of this protection is not clearly understood. The aim of this study was to establish a cell culture-based model of damage to C2C12 skeletal muscle cells using the calcium ionophore, A23187 and the mitochondrial uncoupler, 2,4-dinitrophenol (DNP) as damaging agents. Treatment of cells with 1 mM DNP for 60 min resulted in the release of 63.5 % of intracellular creatine kinase (CK) activity over the 3 h experimental period. Treatment of cells with 10 microM A23187 for 30 min resulted in the release of 47.9 % of CK activity. Exposure of myotubes to a period of hyperthermia resulted in a significant increase in their content of HSP25, HSP60, HSC70 (heat shock cognate) and HSP70. This increase in HSPs was associated with significant protection against both DNP-induced and A23187-induced damage to the myotubes. These results indicate that an increased content of HSPs may provide protection against the muscle damage that occurs by a pathological increase in intracellular calcium or uncoupling of the mitochondrial respiratory chain.
Authors:
A A Maglara; A Vasilaki; M J Jackson; A McArdle
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2003-02-21
Journal Detail:
Title:  The Journal of physiology     Volume:  548     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2003 May 
Date Detail:
Created Date:  2003-05-01     Completed Date:  2004-08-19     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  837-46     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of Liverpool, Liverpool L69 3GA, UK.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcimycin / pharmacology
Calcium / metabolism
Cell Line
Cell Survival / drug effects
Cells, Cultured
Chaperonin 60 / physiology
Cold Temperature
Creatine Kinase / metabolism
Energy Metabolism
HSP70 Heat-Shock Proteins / physiology
Heat-Shock Proteins / biosynthesis,  physiology*
Homeostasis
Kinetics
Mice
Models, Biological
Muscle Fibers, Skeletal / drug effects,  pathology*,  physiology
Muscle, Skeletal / drug effects,  pathology*,  physiology
Chemical
Reg. No./Substance:
0/Chaperonin 60; 0/HSP70 Heat-Shock Proteins; 0/Heat-Shock Proteins; 52665-69-7/Calcimycin; 7440-70-2/Calcium; EC 2.7.3.2/Creatine Kinase
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