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# A role for caveolin-3 in the pathogenesis of the mdx mouse

Larner, Dean Paul (2012)
Ph.D. thesis, University of Birmingham.

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## Abstract

Duchenne muscular dystrophy (DMD) is a muscle-wasting disease caused by the loss of sarcolemmal protein dystrophin. In DMD and the mouse model of the disease mdx, there is an increase in an associated protein, caveolin-3. In this study, mdx mice with deficiencies in caveolin-3 were generated to allow a distinction to be made between the pathology caused by the loss of dystrophin and that caused by an excess of caveolin-3.

It was found that in late gestation embryos, there were perturbations in skeletal muscle stem cell populations and depletion of respiratory muscles in mdx and mdx/cav3$$^{+/-}$$, both of which were more severe in mdx/cav3$$^{+/-}$$ embryos. In post natal skeletal muscles, there was a trend in that the level of regeneration, believed to be indicative of previous degeneration, was consistently greater in mdx than mdx/cav3$$^{+/-}$$. Taken together it would appear whereas increased caveolin-3 may compensate for the lack of dystrophin in embryonic mdx muscle; post natally, it may contribute to the muscle regeneration observed in mdx.

The data presented in this thesis should help towards clarifying the contribution of caveolin-3 in the pathogenesis of DMD and in doing so expand on the understanding of the molecular aetiology of the disease.

Type of Work: Ph.D. thesis. Smith, Janet Colleges (2008 onwards) > College of Life & Environmental Sciences School of Biosciences QH301 BiologyRB Pathology University of Birmingham 3244
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