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A Cellular and Molecular Investigation of Dilated Cardiomyopathy (DCM) in Dogs

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dc.contributor.advisor Pyle, Glen
dc.contributor.author Sinclair, Elizabeth
dc.date.accessioned 2013-01-11T19:27:50Z
dc.date.available 2013-01-11T19:27:50Z
dc.date.copyright 2012-12
dc.date.created 2013-01-08
dc.date.issued 2013-01-11
dc.identifier.uri http://hdl.handle.net/10214/5292
dc.description.abstract We hypothesized that alterations in cardiac myofilaments are associated with hereditary canine DCM. DCM myofilaments demonstrated a reduction in EC50 and a modest decrease in maximum activity compared to non-failing dog samples. Treatment of myofilaments with the calcium sensitizer, bepridil, showed a reduction in EC50. Desmin and tropomyosin phosphorylation was increased in DCM. Desmin protein levels were increased in DCM. Total troponin I phosphorylation was unchanged, but S23/S24 phosphorylation was reduced in DCM. Myofilament-associated PKC-δ and -ζ were elevated in DCM, PKC- ε was modestly reduced, and PKC-α showed no change. These data are the first investigation of cardiac myofilaments in naturally occurring canine DCM, and support the hypothesis that alterations in cardiac myofilaments are associated with DCM. en_US
dc.description.sponsorship OVC Pet Trust (operating funds) en_US
dc.language.iso en en_US
dc.subject dilated cardiomyopathy en_US
dc.subject dcm en_US
dc.subject dogs en_US
dc.subject atpase en_US
dc.subject myofilament en_US
dc.subject phosphorylation en_US
dc.subject protein kinase en_US
dc.subject calcium sensitizer en_US
dc.title A Cellular and Molecular Investigation of Dilated Cardiomyopathy (DCM) in Dogs en_US
dc.type Thesis en_US
dc.degree.programme Biomedical Sciences en_US
dc.degree.name Master of Science en_US
dc.degree.department Department of Biomedical Sciences en_US
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