Journal of Applied Physiology
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J Appl Physiol 93: 537-545, 2002. First published April 19, 2002; doi:10.1152/japplphysiol.00202.2002
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Vol. 93, Issue 2, 537-545, August 2002

Regenerated mdx mouse skeletal muscle shows differential mRNA expression

B. S. Tseng1,*, P. Zhao2,*, J. S. Pattison3,*, S. E. Gordon3, J. A. Granchelli4, R. W. Madsen5, L. C. Folk6, E. P. Hoffman2, and F. W. Booth3

1 Division of Child Neurology, Department of Neurology, University of California at San Francisco, San Francisco, California 94143; 2 Research Center for Genetic Medicine, Children's National Medical Center, Washington, District of Columbia 20010; Departments of 3 Veterinary Biomedical Sciences, 5 Statistics, and 6 Veterinary Pathobiology, University of Missouri at Columbia, Columbia, Missouri 65211; and 4 Department of Biological Sciences, State University of New York at Buffalo, Buffalo, New York 14260-1300

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 present 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, despite the absence of a functional dystrophin protein. A number of transcripts whose levels differed between the mdx and human Duchenne muscular dystrophy were noted. A fourfold 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.

Duchenne muscular dystrophy; dystrophin; GeneChips; microarrays

* B. S. Tseng, P. Zhao, and J. S. Pattison contributed equally to this work.




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