ArticlePloS one2013
Mutation types and aging differently affect revertant fiber expansion in dystrophic mdx and mdx52 mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Myonuclear Domain-Associated and Central Nucleation-Dependent Spatial Restriction of Dystrophin Protein Expression.Journal of cachexia, sarcopenia and muscle · 2026Article
- Preclinical evaluation of INS1201 AAV9-micro-dystrophin via CSF administration as a potential therapy for Duchenne muscular dystrophy.Molecular therapy. Advances · 2026Article
- Evolution and Breakthroughs in Exon Skipping and Splice Modulation: From Inception to Clinical Success.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Deletion of miR-146a enhances therapeutic protein restoration in model of dystrophin exon skipping.Molecular therapy. Nucleic acids · 2024Article
- Severe cardiac and skeletal manifestations in DMD-edited microminipigs: an advanced surrogate for Duchenne muscular dystrophy.Communications biology · 2024Article
- Break Down of the Complexity and Inconsistency Between Levels of Matriglycan and Disease Phenotype in FKRP-Related Dystroglycanopathies: A Review and Model of Interpretation.Journal of neuromuscular diseases · 2024Review
- Dystrophin myonuclear domain restoration governs treatment efficacy in dystrophic muscle.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Histological Methods to Assess Skeletal Muscle Degeneration and Regeneration in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2022Review
- Enhanced exon skipping and prolonged dystrophin restoration achieved by TfR1-targeted delivery of antisense oligonucleotide using FORCE conjugation in mdx mice.Nucleic acids research · 2022Article
- Comparison of dystrophin expression following gene editing and gene replacement in an aged preclinical DMD animal model.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Loss of Nup210 results in muscle repair delays and age-associated alterations in muscle integrity.Life science alliance · 2022Article
- The skeletal muscle phenotype of the DE50-MD dog model of Duchenne muscular dystrophy.Wellcome open research · 2022Article
- AInternational journal of molecular sciences · 2021Article
- Mutation-independent Proteomic Signatures of Pathological Progression in Murine Models of Duchenne Muscular Dystrophy.Molecular & cellular proteomics : MCP · 2020Article
- Morpholino-induced exon skipping stimulates cell-mediated and humoral responses to dystrophin in mdx mice.The Journal of pathology · 2019Article
- Greater Colo-Rectal Activation Phenotype in Exercised mdx Mice.PLoS currents · 2018Article
- Humanizing the mdx mouse model of DMD: the long and the short of it.NPJ Regenerative medicine · 2018Review
- Quantitative Antisense Screening and Optimization for Exon 51 Skipping in Duchenne Muscular Dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Impaired regenerative capacity and lower revertant fibre expansion in dystrophin-deficient mdx muscles on DBA/2 background.Scientific reports · 2016Article
- Current Translational Research and Murine Models For Duchenne Muscular Dystrophy.Journal of neuromuscular diseases · 2016Review
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD), one of the most common and lethal genetic disorders, and the mdx mouse myopathies are caused by a lack of dystrophin protein. These dystrophic muscles contain sporadic clusters of dystrophin-expressing revertant fibers (RFs), as detected by immunohistochemistry. RFs are known to arise from muscle precursor cells with spontaneous exon skipping (alternative splicing) and clonally expand in size with increasing age through the process of muscle degeneration/regeneration. The expansion of revertant clusters is thought to represent the cumulative history of muscle regeneration and proliferation of such precursor cells. However, the precise mechanisms by which RFs arise and expand are poorly understood. Here, to test the effects of mutation types and aging on RF expansion and muscle regeneration, we examined the number of RFs in mdx mice (containing a nonsense mutation in exon 23) and mdx52 mice (containing deletion mutation of exon 52) with the same C57BL/6 background at 2, 6, 12, and 18months of age. Mdx mice displayed a significantly higher number of RFs compared to mdx52 mice in all age groups, suggesting that revertant fiber expansion largely depends on the type of mutation and/or location in the gene. A significant increase in the expression and clustering levels of RFs was found beginning at 6months of age in mdx mice compared with mdx52 mice. In contrast to the significant expansion of RFs with increasing age, the number of centrally nucleated fibers and embryonic myosin heavy chain-positive fibers (indicative of cumulative and current muscle regeneration, respectively) decreased with age in both mouse strains. These results suggest that mutation types and aging differently affect revertant fiber expansion in mdx and mdx52 mice.
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