ArticleThe Journal of physiology2008
CC family chemokines directly regulate myoblast responses to skeletal muscle injury.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 129 citations in OpenAlex.
- The effects of cold water immersion and active recovery on inflammation and cell stress responses in human skeletal muscle after resistance exercise.The Journal of physiology · 2017Trial
- Review
- CXCL14 Enhances Myocyte Fusion and Activates the FAK-ERK5 Signaling Pathway in Skeletal Muscle Stem Cells and Myoblasts.International journal of stem cells · 2026Article
- Regulatory T cell attracting therapy accelerates skeletal muscle functional recovery following injury.Scientific reports · 2026Article
- Transcriptome analysis of injured muscle identifies new candidate genes for satellite cell growth and myofiber formation during early muscle regeneration.Animal bioscience · 2026Article
- Repeated bouts of load carriage alter indirect markers of exercise-induced muscle damage, liver enzymes, and oxygen-carrying capacity in male soldiers.Physiological reports · 2025Article
- Anti-myogenic and profibrotic effect of serum from patients affected by muscular laminopathies.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2025Article
- Skeletal muscle stem cells modulate niche function in Duchenne muscular dystrophy mouse through YY1-CCL5 axis.Nature communications · 2025Article
- Temporal dynamics of gene and protein signatures following volumetric muscle loss.Frontiers in cell and developmental biology · 2025Article
- Fibro-adipogenic progenitor cells in skeletal muscle unloading: metabolic and functional impairments.Skeletal muscle · 2024Article
- The MyoGravity project to study real microgravity effects on human muscle precursor cells and tissue.NPJ microgravity · 2024Article
- Muscle cell-derived Ccl8 is a negative regulator of skeletal muscle regeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Article
- Evaluation of a six-minute walk test in the DE50-MD canine model of Duchenne muscular dystrophy and its effect on blood-borne biomarkers.Wellcome open research · 2024Article
- Insulin resistance and dyslipidemia in low-birth-weight goat kids.Frontiers in veterinary science · 2024Article
- Single cell analysis reveals satellite cell heterogeneity for proinflammatory chemokine expression.Frontiers in cell and developmental biology · 2023Article
- A conciseFrontiers in cell and developmental biology · 2023Article
- Serum inflammatory cytokines as disease biomarkers in the DE50-MD dog model of Duchenne muscular dystrophy.Disease models & mechanisms · 2022Article
- Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022Review
- Wharton's Jelly-Derived Mesenchymal Stem Cells with High Aurora Kinase A Expression Show Improved Proliferation, Migration, and Therapeutic Potential.Stem cells international · 2022Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemokines have been implicated in the promotion of leucocyte trafficking to diseased muscle. The purpose of this study was to determine whether a subset of inflammatory chemokines are able to directly drive myoblast proliferation, an essential early component of muscle regeneration, in a manner which is entirely independent of leucocytes. Cultured myoblasts (C2C12) were exposed to monocyte chemoattractant protein-1 (MCP-1; CCL2), macrophage inflammatory protein-1alpha (MIP-1alpha; CCL3) or MIP-1beta (CCL4). All chemokines induced phosphorylation of extracellular signal-regulated kinase (ERK)1/2 mitogen-activated protein kinase (MAPK) and greatly increased myoblast proliferative responses. Chemokine-induced myoblast proliferation was abolished by pertussis toxin and the MEK1/2 inhibitor U0126, implicating both Galphai-coupled receptors and ERK1/2-dependent signalling. Myoblasts expressed receptors for all of the chemokines tested, and mitogenic responses were specifically inhibited by antibodies directed against CC family chemokine receptors 2 and 5 (CCR2 and CCR5). Within an in vitro myogenic wound healing assay devoid of leucocytes, all chemokines significantly accelerated the time course of myoblast wound closure after mechanical injury. Injections of MCP-1 into cardiotoxin-injured skeletal muscles in vivo also suppressed expression of the differentiation marker myogenin, consistent with a mitogenic effect. Taken together, our results indicate that CC chemokines have potent and direct effects on myoblast behaviour, thus indicating a novel role in muscle repair beyond leucocyte chemoattraction. Therefore, interventions aimed at modulating the balance between myoblast and leucocyte effects of CC chemokines in injured muscle could represent a novel strategy for the treatment of destructive muscle pathologies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.