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IL-10 Triggers Changes in Macrophage Phenotype That Promote Muscle Growth and Regeneration
Open accessAbstract
We examined the function of IL-10 in regulating changes in macrophage phenotype during muscle growth and regeneration following injury. Our findings showed that the Th1 cytokine response in inflamed muscle is characterized by high levels of expression of CD68, CCL-2, TNF-α, and IL-6 at 1 d postinjury. During transition to the Th2 cytokine response, expression of those transcripts declined, whereas CD163, IL-10, IL-10R1, and arginase-1 increased. Ablation of IL-10 amplified the Th1 response at 1 d postinjury, causing increases in IL-6 and CCL2, while preventing a subsequent increase in CD163 and arginase-1. Reductions in muscle fiber damage that normally occurred between 1 and 4 d postinjury did not occur in IL-10 mutants. In addition, muscle regeneration and growth were greatly slowed by loss of IL-10. Furthermore, myogenin expression increased in IL-10 mutant muscle at 1 d postinjury, suggesting that the mutation amplified the transition from the proliferative to the early differentiation stages of myogenesis. In vitro assays showed that stimulation of muscle cells with IL-10 had no effect on cell proliferation or expression of MyoD or myogenin. However, coculturing muscle cells with macrophages activated with IL-10 to the M2 phenotype increased myoblast proliferation without affecting MyoD or myogenin expression, showing that M2 macrophages promote the early, proliferative stage of myogenesis. Collectively, these data show that IL-10 plays a central role in regulating the switch of muscle macrophages from a M1 to M2 phenotype in injured muscle in vivo, and this transition is necessary for normal growth and regeneration of muscle.
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“In mouse skeletal muscle injury by chemical toxin or unloading/reloading, IL-4 mRNA, although detectable, does not rise above uninjured levels over the course of healing [73,74].”
From Macrophage phenotypes during tissue repair (2013) · cites this paper as [73]
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Metadata
- Authors
- Deng, B., Wehling-Henricks, M., Villalta, S. A., Wang, Y., & Tidball, J. G.
- Affiliations
- University of California, Los Angeles (US)
- Department of Integrative Biology and Physiology, University of California , Los Angeles, Los Angeles, CA 90095
- Corresponding author
- Deng, Bo
- Wang, Ying
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-10-01
- Volume
- 189
- Issue
- 7
- Pages
- 3669-3680
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3448810
- OpenAlex
- W2153554828
- Cited by
- 472
- References
- 68
- Citations by year
- 2026: 24 · 2025: 25 · 2024: 26 · 2023: 33 · 2022: 43 · 2021: 40 · 2020: 41 · 2019: 44 · 2018: 32 · 2017: 43 · 2016: 43 · 2015: 28 · 2014: 27 · 2013: 22 · 2012: 1
- FWCI
- 9.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Muscular Dystrophy Association (157881)
- National Institutes of Health (R01 AR/AG054451)
- National Institute on Aging (R01 AR/AG054451)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR047855, R01AR054451, R01AR047721)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Surgery › Wound Healing and Treatments
- Keywords
- IL-10, muscle regeneration, muscle growth, macrophage polarization, M2 macrophages, M1 macrophages, Th1/Th2 shift, muscle damage, myogenesis, myoblast proliferation, arginase-1, CD163, myogenin, MyoD, MCP-1, TNF-α, interleukin-6
- MeSH terms
- Animals, Female, Macrophages, Mice, Inbred C57BL, Regeneration, Up-Regulation, Immunophenotyping, Cytokines, Interleukin-10, Mice, Knockout, Th1 Cells, Th2 Cells, Muscle, Skeletal, Cell Enlargement, Cell Proliferation, Mice, Mice, 129 Strain
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