Diseased muscles that lack dystrophin or laminin-α2 have altered compositions and proliferation of mononuclear cell populations
| Autor: | Christine A. Kostek, Jeffrey Boone Miller, Mahasweta Girgenrath |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2005 |
| Předmět: |
Pathology
medicine.medical_specialty Clinical Neurology Cell Count lcsh:RC346-429 Dystrophin 03 medical and health sciences Mice 0302 clinical medicine Multinucleate Muscular Diseases Laminin Precursor cell medicine Myocyte Animals Antigens Ly Muscle Skeletal lcsh:Neurology. Diseases of the nervous system 030304 developmental biology Cell Proliferation Mice Knockout 0303 health sciences Analysis of Variance Muscle Cells biology Cell growth business.industry Age Factors Skeletal muscle Membrane Proteins General Medicine Cell sorting Flow Cytometry Cell biology Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure Bromodeoxyuridine Gene Expression Regulation biology.protein Mice Inbred mdx Leukocyte Common Antigens Neurology (clinical) business 030217 neurology & neurosurgery Research Article |
| Zdroj: | BMC Neurology BMC Neurology, Vol 5, Iss 1, p 7 (2005) |
| ISSN: | 1471-2377 |
| Popis: | Background Multiple 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-α2-deficiency, altered the proliferation and composition of different subsets of muscle-derived mononucleate cells. Methods We 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-α2-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. Results We found that the proliferation and composition of the mononucleate cells in dystrophin-deficient and laminin-α2-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. Conclusion The 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. |
| Databáze: | OpenAIRE |
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