ArticleEuropean journal of applied physiology2011
Proteomic assessment of the acute phase of dystrophin deficiency in mdx mice.
Article in European journal of applied physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 50 citations in OpenAlex.
- How Can Proteomics Help to Elucidate the Pathophysiological Crosstalk in Muscular Dystrophy and Associated Multi-System Dysfunction?Proteomes · 2024Article
- Comparative 3-Sample 2D-DIGE Analysis of Skeletal Muscles.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Proteomic profiling of impaired excitation-contraction coupling and abnormal calcium handling in muscular dystrophy.Proteomics · 2022Review
- Reducing sarcolipin expression improves muscle metabolism inAmerican journal of physiology. Cell physiology · 2022Article
- Mutation-independent Proteomic Signatures of Pathological Progression in Murine Models of Duchenne Muscular Dystrophy.Molecular & cellular proteomics : MCP · 2020Article
- PGC-1α overexpression increases transcription factor EB nuclear localization and lysosome abundance in dystrophin-deficient skeletal muscle.Physiological reports · 2020Article
- Dystrophinopathy-associated dysfunction of Krebs cycle metabolism.Human molecular genetics · 2019Article
- [Molecular pathogenesis of Duchenne muscular dystrophy-related fibrosis].Der Pathologe · 2017Article
- Progressive muscle proteome changes in a clinically relevant pig model of Duchenne muscular dystrophy.Scientific reports · 2016Article
- The biochemical and mass spectrometric profiling of the dystrophin complexome from skeletal muscle.Computational and structural biotechnology journal · 2016Review
- Concurrent Label-Free Mass Spectrometric Analysis of Dystrophin Isoform Dp427 and the Myofibrosis Marker Collagen in Crude Extracts fromProteomes · 2015Article
- Circulating Biomarkers for Duchenne Muscular Dystrophy.Journal of neuromuscular diseases · 2015Article
- Comparative Label-Free Mass Spectrometric Analysis of Mildly versus Severely Affected mdx Mouse Skeletal Muscles Identifies Annexin, Lamin, and Vimentin as Universal Dystrophic Markers.Molecules (Basel, Switzerland) · 2015Article
- Article
- Reduction in mdx mouse muscle degeneration by low-intensity endurance exercise: a proteomic analysis in quadriceps muscle of exercised compared with sedentary mdx mice.Bioscience reports · 2015Article
- Quantitative proteomic analysis reveals metabolic alterations, calcium dysregulation, and increased expression of extracellular matrix proteins in laminin α2 chain-deficient muscle.Molecular & cellular proteomics : MCP · 2014Article
- Affinity proteomics within rare diseases: a BIO-NMD study for blood biomarkers of muscular dystrophies.EMBO molecular medicine · 2014Article
- Proteomic profiling of the dystrophin-deficient mdx phenocopy of dystrophinopathy-associated cardiomyopathy.BioMed research international · 2014Review
- New pathobiochemical insights into dystrophinopathy from the proteomics of senescent mdx mouse muscle.Frontiers in aging neuroscience · 2014Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is caused by the absence of a functional dystrophin protein and is modeled by the mdx mouse. The mdx mouse suffers an early necrotic bout in the hind limb muscles lasting from approximately 4 to 7 weeks. The purpose of this investigation was to determine the extent to which dystrophin deficiency changed the proteome very early in the disease process. In order to accomplish this, proteins from gastrocnemius from 6-week-old C57 (n = 6) and mdx (n = 6) mice were labeled with fluorescent dye and subjected to two-dimensional differential in-gel electrophoresis (2D-DIGE). Resulting differentially expressed spots were excised and protein identity determined via MALDI-TOF followed by database searching using MASCOT. Proteins of the immediate energy system and glycolysis were generally down-regulated in mdx mice compared to C57 mice. Conversely, expression of proteins involved in the Kreb's cycle and electron transport chain were increased in dystrophin-deficient muscle compared to control. Expression of cytoskeletal components, including tubulins, vimentin, and collagen, were increased in mdx mice compared to C57 mice. Importantly, these changes are occurring at only 6 weeks of age and are caused by acute dystrophin deficiency rather than more chronic injury. These data may provide insight regarding early pathologic changes occurring in dystrophin-deficient skeletal muscle.
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