Document Detail


The physiological effects of IGF-1 (class 1:Ea transgene) over-expression on exercise-induced damage and adaptation in dystrophic muscles of mdx mice.
MedLine Citation:
PMID:  18726613     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Duchenne muscular dystrophy (DMD) is a genetic disorder in which muscle weakness and fragility contribute to ongoing muscle degeneration. Although exercise-induced muscle damage is associated with adaptation that protects normal muscle from further damage, exploiting this process to protect dystrophic muscle has been avoided for fear of inducing excessive muscle degeneration. However, muscle-specific over-expression of the class 1:Ea isoform of insulin-like growth factor-1 (IGF-1) reduces myofibre necrosis in dystrophic mdx mice (a model for DMD) and, therefore, may enhance the adaptation process in response to eccentric exercise. To test this hypothesis, we evaluated the effect of transgenic class 1:Ea IGF-1 over-expression on the susceptibility to muscle damage and subsequent adaptation in 12-week-old dystrophic mdx and non-dystrophic control mice. Experiments were conducted in vivo using a custom-built isokinetic mouse dynamometer to measure the deficit in joint torque (indicating muscle damage) after 20 maximal lengthening (eccentric) contractions. Adaptation to this damaging exercise was evaluated by repeating the protocol 7 days after the initial exercise. The over-expression of IGF-1 significantly increased the normalised joint torque in non-dystrophic mice and appeared to ameliorate the muscle weakness in dystrophic mice. All mice displayed a marked reduction in the susceptibility to muscle damage on day 7; however, this adaptation was unaffected by IGF-1, showing that IGF-1 does not protect the dystrophic muscles of adult mdx mice against damage resulting from maximal lengthening contractions.
Authors:
James A Ridgley; Gavin J Pinniger; Peter W Hamer; Miranda D Grounds
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-08-26
Journal Detail:
Title:  Pflügers Archiv : European journal of physiology     Volume:  457     ISSN:  1432-2013     ISO Abbreviation:  Pflugers Arch.     Publication Date:  2009 Mar 
Date Detail:
Created Date:  2009-02-09     Completed Date:  2009-07-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0154720     Medline TA:  Pflugers Arch     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  1121-32     Citation Subset:  IM    
Affiliation:
The University of Western Australia, Crawley, Australia.
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MeSH Terms
Descriptor/Qualifier:
Animals
Disease Models, Animal
Gene Expression
Gene Therapy
Insulin-Like Growth Factor I / genetics,  physiology*,  therapeutic use
Male
Mice
Mice, Inbred mdx
Mice, Transgenic
Muscle Contraction
Muscle Fatigue
Muscle, Skeletal / pathology,  physiopathology
Muscular Dystrophy, Animal / therapy*
Muscular Dystrophy, Duchenne / therapy*
Physical Exertion / physiology
Transgenes*
Chemical
Reg. No./Substance:
67763-96-6/Insulin-Like Growth Factor I

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


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