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Articles in PresS, published online ahead of print April 19, 2002
J Appl Physiol, 10.1152/jap.00202.2002
Submitted on March 11, 2002
Accepted on April 15, 2002
1 Department of Neurology, Division of Child Neurology, University of California, San Francisco, CA, USA
2 Research Center for Genetic Medicine, Children's National Medical Center, Washington, DC, USA
3 Department of Veterinary Biomedical Sciences, University of Missouri at Columbia, Columbia, MO, USA
4 Department of Biological Sciences, State University of New York at Buffalo, Buffalo, NY, USA
5 Department of Statistics, Univeristy of Missouri at Columbia, Columbia, MO, USA
6 Department of Veterinary Pathobiology, University of Missouri at Columbia, Columbia, MO, USA
* To whom correspondence should be addressed. E-mail: boothf{at}missouri.edu.
Despite over 3,000 articles published on dystrophin in the last 15 years, the reasons underlying the progression of the human disease, differential muscle involvement, and disparate phenotypes in different species are not understood. The current experiment employed a screen of 12,488 mRNAs in 16-wk-old mouse mdx muscle at a time when the skeletal muscle is avoiding severe dystrophic pathophysiology in spite of the absence of a functional dystrophin protein. A number of transcripts whose levels differed between the mdx and human Duchenne muscular dystrophy (DMD) were noted. A 4-fold decrease in myostatin mRNA in the mdx muscle was noted. Differential upregulation of actin-related protein 2/3 (subunit 4), [beta]-thymosin, calponin, mast cell chymase, and guanidinoacetate methyltransferase mRNA in the more benign mdx was also observed. Transcripts for oxidative and glycolytic enzymes in mdx muscle were not downregulated. These discrepancies could provide candidates for salvage pathways that maintain skeletal muscle integrity in the absence of a functional dystrophin protein in mdx skeletal muscle.
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