Use this URL to cite or link to this record in EThOS: | https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.549151 |
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Title: | A role for caveolin-3 in the pathogenesis of the mdx mouse | ||||||
Author: | Larner, Dean Paul |
ISNI:
0000 0004 2714 7299
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Awarding Body: | University of Birmingham | ||||||
Current Institution: | University of Birmingham | ||||||
Date of Award: | 2012 | ||||||
Availability of Full Text: |
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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.
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Supervisor: | Not available | Sponsor: | BBSRC | ||||
Qualification Name: | Thesis (Ph.D.) | Qualification Level: | Doctoral | ||||
EThOS ID: | uk.bl.ethos.549151 | DOI: | Not available | ||||
Keywords: | QH301 Biology ; RB Pathology | ||||||
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