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Am J Physiol Cell Physiol (May 29, 2002). doi:10.1152/ajpcell.00450.2001
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Articles in PresS, published online ahead of print May 29, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00450.2001
Submitted on September 19, 2001
Accepted on May 22, 2002

Fast-twitch skeletal muscles of dystrophic mouse pups are resistant to injury from acute mechanical stress

Robert W. Grange1*, Thomas G. Gainer1, Krista M. Marschner1, Robert J. Talmadge1, and James T. Stull2

1 Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA
2 Physiology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA

* To whom correspondence should be addressed. E-mail: rgrange{at}vt.edu.

Loss of the dystrophin-glycoprotein complex from muscle sarcolemma in Duchenne's Muscular Dystrophy (DMD) renders the membrane susceptible to mechanical injury, leaky to Ca2+ and disrupts signaling, but the precise mechanism(s) leading to onset of DMD remain unclear. To assess the role of mechanical injury in onset of DMD, EDL muscles from C57 (control), mdx and mdx:utrophin-deficient (mdx:utrn-/-; dystrophic) pups aged 9-12 days, were subjected to an acute stretch-injury or no-stretch protocol in vitro. Before the stretches, isometric stress was attenuated for mdx:utrn-/- compared to control muscles at all stimulation frequencies (p <0.05). During the stretches, EDL muscles for each genotype demonstrated similar mean stiffness values. Following the stretches, isometric stress during a tetanus was significantly decreased for both mdx and mdx:utrn-/- muscles compared to control muscles (p<0.05). Membrane injury assessed by uptake of procion orange dye was greater for dystrophic compared to control EDL (p<0.05), but within each genotype, percent of total cells taking up dye was not different for the no-stretch vs. stretch condition. These data suggest that the sarcolemma of maturing dystrophic EDL muscles are resistant to acute mechanical injury.




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