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Lookup NU author(s): Stephanie Carr, Professor Hanns Lochmuller, Dr Andreas Roos
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© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. Duchenne muscular dystrophy (DMD) is a genetic muscle wasting condition with limited treatment options available and is caused by the lack of dystrophin. However, pathophysiology of different tissues is variable showing different histological and molecular signatures. Recently, a number of studies have employed gel-free proteomic approaches to unveil the molecular pathophysiology in terms of tissue-specific proteome changes in dystrophin deficiency. The authors analyzed studies in models of dystrophin deficiency and patients both from the published literature. The authors created a database containing all of the significantly differentially expressed proteins. By the integration of data from nine studies, the authors have identified 31 proteins which are commonly affected in different tissues by dystrophin deficiency. These proteins represent pathways involved in the maintenance of the actin cytoskeleton and those involved in cellular energy metabolism among others. Also represented is glyceraldehyde-3-phosphate dehydrogenase (GAPDH), often used as a loading control in protein assays, it appears to be highly variable, and should be replaced by other controls. The same intersection of data was performed using studies of the blood and urine of Duchenne muscular dystrophy patients and/or animal models and identified 33 proteins that are commonly differentially expressed. These proteins may themselves be novel therapeutic targets biomarkers that could monitor disease progression.
Author(s): Carr SJ, Zahedi RP, Lochmuller H, Roos A
Publication type: Article
Publication status: Published
Journal: Proteomics - Clinical Applications
Year: 2018
Volume: 12
Issue: 2
Print publication date: 01/03/2018
Online publication date: 20/06/2017
Acceptance date: 14/06/2017
ISSN (print): 1862-8346
ISSN (electronic): 1862-8354
Publisher: Wiley-VCH Verlag
URL: https://doi.org/10.1002/prca.201700071
DOI: 10.1002/prca.201700071
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