ArticleBMC neurology2005
Diseased muscles that lack dystrophin or laminin-alpha2 have altered compositions and proliferation of mononuclear cell populations.
Article in BMC neurology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Defining and identifying satellite cell-opathies within muscular dystrophies and myopathies.Experimental cell research · 2022Article
- Impaired Regeneration in Dystrophic Muscle-New Target for Therapy.Frontiers in molecular neuroscience · 2020Article
- A Family of Laminin α2 Chain-Deficient Mouse Mutants: Advancing the Research on LAMA2-CMD.Frontiers in molecular neuroscience · 2020Review
- Early skeletal muscle pathology and disease progress in the dyScientific reports · 2019Article
- Pharyngeal Satellite Cells Undergo Myogenesis Under Basal Conditions and Are Required for Pharyngeal Muscle Maintenance.Stem cells (Dayton, Ohio) · 2015Article
- A splice site mutation in laminin-α2 results in a severe muscular dystrophy and growth abnormalities in zebrafish.PloS one · 2012Article
- Muscle-specific expression of insulin-like growth factor 1 improves outcome in Lama2Dy-w mice, a model for congenital muscular dystrophy type 1A.Human molecular genetics · 2011Article
- Pathology is alleviated by doxycycline in a laminin-alpha2-null model of congenital muscular dystrophy.Annals of neurology · 2009Article
- TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration.The EMBO journal · 2006Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMultiple types of mononucleate cells reside among the multinucleate myofibers in skeletal muscles and these mononucleate cells function in muscle maintenance and repair. How neuromuscular disease might affect different types of muscle mononucleate cells had not been determined. In this study, therefore, we examined how two neuromuscular diseases, dystrophin-deficiency and laminin-alpha2-deficiency, altered the proliferation and composition of different subsets of muscle-derived mononucleate cells.
methodsWe used fluorescence-activated cell sorting combined with bromodeoxyuridine labeling to examine proliferation rates and compositions of mononuclear cells in diseased and healthy mouse skeletal muscle. We prepared mononucleate cells from muscles of mdx (dystrophin-deficient) or Lama2-/- (laminin-alpha2-deficient) mice and compared them to cells from healthy control muscles. We enumerated subsets of resident muscle cells based on Sca-1 and CD45 expression patterns and determined the proliferation of each cell subset in vivo by BrdU incorporation.
resultsWe found that the proliferation and composition of the mononucleate cells in dystrophin-deficient and laminin-alpha2-deficient diseased muscles are different than in healthy muscle. The mdx and Lama2-/- muscles showed similar significant increases in CD45+ cells compared to healthy muscle. Changes in proliferation, however, differed between the two diseases with proliferation increased in mdx and decreased in Lama2-/- muscles compared to healthy muscles. In particular, the most abundant Sca-1-/CD45- subset, which contains muscle precursor cells, had increased proliferation in mdx muscle but decreased proliferation in Lama2-/- muscles.
conclusionThe similar increases in CD45+ cells, but opposite changes in proliferation of muscle precursor cells, may underlie aspects of the distinct pathologies in the two diseases.
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