Skip Navigation



Human Molecular Genetics Advance Access published online on September 16, 2008
Human Molecular Genetics, doi:10.1093/hmg/ddn301
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Data
Right arrow All Versions of this Article:
17/24/3975    most recent
ddn301v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Banks, G. B
Right arrow Articles by Chamberlain, J. S
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Banks, G. B
Right arrow Articles by Chamberlain, J. S
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 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, Seattle, Washington 98195, USA 2 Department of Medicine , and Department of Biochemistry, Seattle, Washington 98195, USA 3 University of Washington, Seattle, Washington 98195, USA

* Corresponding Author: Professor Jeffrey S Chamberlain. Jeffrey S. Chamberlain, Ph.D. (Corresponding author), Professor of Neurology, Medicine and Biochemistry, Director, Senator Paul D. Wellstone Muscular Dystrophy Cooperative Research Center, Rm K243b HSB, Box 357720, University of Washington School of Medicine, 1959 NE Pacific Street, Seattle, Washington, 98195-7720, Phone: 206-616-6645, Fax: 206-616-8272, 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. While 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 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 prevent muscle necrosis and retain the function of necessary muscles during injury, ageing and disease.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Pathol.Home page
J. V. Welser, J. E. Rooney, N. C. Cohen, P. B. Gurpur, C. A. Singer, R. A. Evans, B. A. Haines, and D. J. Burkin
Myotendinous Junction Defects and Reduced Force Transmission in Mice that Lack {alpha}7 Integrin and Utrophin
Am. J. Pathol., October 1, 2009; 175(4): 1545 - 1554.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.