Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.

Duchenne Muscular Dystrophy (DMD) is a fatal muscle wasting disorder caused by dystrophin deficiency. Previous work suggested that increased expression of the dystrophin-related protein utrophin in the mdx mouse can reduce the dystrophic pathophysiology. Physiological tests showed that the transgeni...

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Asıl Yazarlar: Baban, D, Davies, K
Materyal Türü: Journal article
Dil:English
Baskı/Yayın Bilgisi: 2008
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author Baban, D
Davies, K
author_facet Baban, D
Davies, K
author_sort Baban, D
collection OXFORD
description Duchenne Muscular Dystrophy (DMD) is a fatal muscle wasting disorder caused by dystrophin deficiency. Previous work suggested that increased expression of the dystrophin-related protein utrophin in the mdx mouse can reduce the dystrophic pathophysiology. Physiological tests showed that the transgenic mouse muscle functioned in a way similar to normal muscle. More recently, it has become possible to analyse disease pathways using microarrays, a sensitive method to evaluate the efficacy of a therapeutic approach. We thus examined the gene expression profile of mdx mouse muscle compared to wild-type mouse muscle and compared the data with that obtained from the transgenic line overexpressing utrophin. The data confirm that the expression of utrophin in the mdx mouse muscle results in a global gene expression profile more similar to that seen for the wild-type mouse. This study confirms that a strategy to up-regulate utrophin is likely to be beneficial in dystrophin deficiency.
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spelling oxford-uuid:db9a7672-f128-4de1-b47f-6f6712d287d62022-03-27T09:11:47ZMicroarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:db9a7672-f128-4de1-b47f-6f6712d287d6EnglishSymplectic Elements at Oxford2008Baban, DDavies, KDuchenne Muscular Dystrophy (DMD) is a fatal muscle wasting disorder caused by dystrophin deficiency. Previous work suggested that increased expression of the dystrophin-related protein utrophin in the mdx mouse can reduce the dystrophic pathophysiology. Physiological tests showed that the transgenic mouse muscle functioned in a way similar to normal muscle. More recently, it has become possible to analyse disease pathways using microarrays, a sensitive method to evaluate the efficacy of a therapeutic approach. We thus examined the gene expression profile of mdx mouse muscle compared to wild-type mouse muscle and compared the data with that obtained from the transgenic line overexpressing utrophin. The data confirm that the expression of utrophin in the mdx mouse muscle results in a global gene expression profile more similar to that seen for the wild-type mouse. This study confirms that a strategy to up-regulate utrophin is likely to be beneficial in dystrophin deficiency.
spellingShingle Baban, D
Davies, K
Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.
title Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.
title_full Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.
title_fullStr Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.
title_full_unstemmed Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.
title_short Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.
title_sort microarray analysis of mdx mice expressing high levels of utrophin therapeutic implications for dystrophin deficiency
work_keys_str_mv AT baband microarrayanalysisofmdxmiceexpressinghighlevelsofutrophintherapeuticimplicationsfordystrophindeficiency
AT daviesk microarrayanalysisofmdxmiceexpressinghighlevelsofutrophintherapeuticimplicationsfordystrophindeficiency