The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index.
Interleukin-10 reduces the pathology of mdx muscular dystrophy by deactivating M1 macrophages and modulating macrophage phenotype
Open accessAbstract
M1 macrophages play a major role in worsening muscle injury in the mdx mouse model of Duchenne muscular dystrophy. However, mdx muscle also contains M2c macrophages that can promote tissue repair, indicating that factors regulating the balance between M1 and M2c phenotypes could influence the severity of the disease. Because interleukin-10 (IL-10) modulates macrophage activation in vitro and its expression is elevated in mdx muscles, we tested whether IL-10 influenced the macrophage phenotype in mdx muscle and whether changes in IL-10 expression affected the pathology of muscular dystrophy. Ablation of IL-10 expression in mdx mice increased muscle damage in vivo and reduced mouse strength. Treating mdx muscle macrophages with IL-10 reduced activation of the M1 phenotype, assessed by iNOS expression, and macrophages from IL-10 null mutant mice were more cytolytic than macrophages isolated from wild-type mice. Our data also showed that muscle cells in mdx muscle expressed the IL-10 receptor, suggesting that IL-10 could have direct effects on muscle cells. We assayed whether ablation of IL-10 in mdx mice affected satellite cell numbers, using Pax7 expression as an index, but found no effect. However, IL-10 mutation significantly increased myogenin expression in vivo during the acute and the regenerative phase of mdx pathology. Together, the results show that IL-10 plays a significant regulatory role in muscular dystrophy that may be caused by reducing M1 macrophage activation and cytotoxicity, increasing M2c macrophage activation and modulating muscle differentiation.
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“Studies have also suggested that macrophage polarization may play an important role in the process of muscle wasting which occurs in models of muscular dystrophy [124,126,127].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [124]
In the citing paper
“The transition to an M2 environment not only serves to attenuate the inflammatory response and potentially cytotoxic production of nitric oxide, but also to drive the differentiation and fusion of cells [114,124].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [124]
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Cites
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Interleukin-10 and the Interleukin-10 Receptor
Moore, K. W., de Waal Malefyt, R., Coffman, R. L., & O'Garra, A. (2001) · Annual Review of Immunology · doi:10.1146/annurev.immunol.19.1.683 · Cited by 6,737
The chemokine system in diverse forms of macrophage activation and polarization
MANTOVANI, A., SICA, A., SOZZANI, S., ALLAVENA, P., VECCHI, A., & LOCATI, M. (2004) · Trends in Immunology · doi:10.1016/j.it.2004.09.015 · Cited by 6,534
Dystrophin: the protein product of the Duchenne muscular dystrophy locus
Hoffman, E. P., Brown, R. H., & Kunkel, L. M. (1987) · Cell · doi:10.1016/0092-8674(87)90579-4 · Cited by 4,693
Macrophage activation and polarization
Martinez, F. O. (2008) · Frontiers in Bioscience · doi:10.2741/2692 · Cited by 3,160
IL-10 inhibits cytokine production by activated macrophages
Fiorentino, D. F., Zlotnik, A., Mosmann, T. R., Howard, M., & O’Garra, A. (1991) · The Journal of Immunology · doi:10.4049/jimmunol.147.11.3815 · Cited by 2,888
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Quantification of mRNA using real-time RT-PCR
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Zanganeh, S., Hutter, G., Spitler, R., Lenkov, O., Mahmoudi, M., Shaw, A., Pajarinen, J. S., Nejadnik, H., Goodman, S., Moseley, M., et al. (2016) · Nature Nanotechnology · doi:10.1038/nnano.2016.168 · Cited by 1,647
Brown, B. N., Ratner, B. D., Goodman, S. B., Amar, S., & Badylak, S. F. (2012) · Biomaterials · doi:10.1016/j.biomaterials.2012.02.034 · Cited by 926
“Studies have also suggested that macrophage polarization may play an important role in the process of muscle wasting which occurs in models of muscular dystrophy [124,126,127].”
BackgroundAberrant repair and fibrosis development in skeletal muscle
Mann, C. J., Perdiguero, E., Kharraz, Y., Aguilar, S., Pessina, P., Serrano, A. L., & Muñoz-Cánoves, P. (2011) · Skeletal Muscle · doi:10.1186/2044-5040-1-21 · Cited by 853
“One example of this was the deletion of IL-10 in mdx mice, which increased muscle damage and reduced muscle strength, due to an imbalance between M1 and M2 macrophages [29].”
BackgroundBrown, B. N., Londono, R., Tottey, S., Zhang, L., Kukla, K. A., Wolf, M. T., Daly, K. A., Reing, J. E., & Badylak, S. F. (2012) · Acta Biomaterialia · doi:10.1016/j.actbio.2011.11.031 · Cited by 745
Regulation of Muscle Growth and Regeneration by the Immune System
Tidball, J. G. (2017) · Nature Reviews Immunology · doi:10.1038/nri.2016.150 · Cited by 740
Self-citation
Metadata
- Authors
- Villalta, S. A., Rinaldi, C., Deng, B., Liu, G., Fedor, B., & Tidball, J. G.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Tidball, J. G.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-11-30
- Volume
- 20
- Issue
- 4
- Pages
- 790-805
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- PMC
- PMC3024048
- OpenAlex
- W2149152441
- Cited by
- 299
- References
- 67
- Citations by year
- 2026: 10 · 2025: 19 · 2024: 11 · 2023: 13 · 2022: 18 · 2021: 20 · 2020: 14 · 2019: 26 · 2018: 25 · 2017: 25 · 2016: 16 · 2015: 24 · 2014: 23 · 2013: 21 · 2012: 21
- FWCI
- 7.17
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Human Molecular Genetics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Muscular Dystrophy Association (157881)
- National Institutes of Health (5r01ar040343-12, AR40343)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR47721, R01 AR 40343, R01AR047721, F31AR054724)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Genetics (clinical) › Neurogenetic and Muscular Disorders Research
- Health Sciences › Medicine › Rheumatology › Inflammatory Myopathies and Dermatomyositis
- Keywords
- IL-10, Duchenne muscular dystrophy, mdx mice, M1 macrophages, M2c macrophages, macrophage polarization, muscle damage, inducible nitric oxide synthase, macrophage cytotoxicity, IL-10 receptor, satellite cells, Pax7, myogenin, muscle regeneration, myogenesis
- MeSH terms
- Animals, Cell Differentiation, Cell Line, Macrophage Activation, Macrophages, Mice, Inbred C57BL, Phagocytosis, Phenotype, Regeneration, Interleukin-10, Mice, Inbred mdx, Muscle, Skeletal, Muscular Dystrophy, Duchenne, Mice, Receptors, Interleukin-10
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