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Human Molecular Genetics Advance Access originally published online on September 16, 2008
Human Molecular Genetics 2008 17(24):3975-3986; doi:10.1093/hmg/ddn301
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Molecular and cellular adaptations to chronic myotendinous strain injury in mdx mice expressing a truncated dystrophin

Glen B. Banks1, Ariana C. Combs1, Joel R. Chamberlain2 and Jeffrey S. Chamberlain1,2,3,*

1 Department of Neurology, Senator Paul D. Wellstone Muscular Dystrophy Cooperative Research Center 2 Department of Medicine 3 Department of Biochemistry, University of Washington, Seattle, WA 98195, USA

* To whom correspondence should be addressed at: Jeffrey S. Chamberlain, Rm K243b HSB, Box 357720, University of Washington School of Medicine, 1959 NE Pacific Street, Seattle, WA 98195-7720, USA. Tel: +1 2066166645; Fax: +1 2066168272; Email: jsc5{at}u.washington.edu

Received June 30, 2008; Revised August 21, 2008; Accepted September 15, 2008

Myotendinous strain injury is the most common injury of human skeletal muscles because the majority of muscle forces are transmitted through this region. Although the immediate response to strain injury is well characterized, the chronic response to myotendinous strain injury is less clear. Here we examined the molecular and cellular adaptations to chronic myotendinous strain injury in mdx mice expressing a microdystrophin transgene (microdystrophin{Delta}R4–R23). We found that muscles with myotendinous strain injury had an increased expression of utrophin and {alpha}7-integrin together with the dramatic restructuring of peripheral myofibrils into concentric rings. The sarcolemma of the microdystrophin{Delta}R4–R23/mdx gastrocnemius muscles was highly protected from experimental lengthening contractions, better than wild-type muscles. We also found a positive correlation between myotendinous strain injury and ringed fibers in the HSALR (human skeletal actin, long repeat) mouse model of myotonic dystrophy. We suggest that changes in protein expression and the formation of rings are adaptations to myotendinous strain injury that help to prevent muscle necrosis and retain the function of necessary muscles during injury, ageing and disease.


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