ArticleSkeletal muscle2015
Upregulated IL-1β in dysferlin-deficient muscle attenuates regeneration by blunting the response to pro-inflammatory macrophages.
Article in Skeletal muscle, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Dysferlin promotes inflammatory macrophage responses and modulates CaLife science alliance · 2026Article
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- Discovery of tissue-specific proteomic signatures in juvenile dermatomyositis highlights pathways reflecting persistent disease activity, clinical heterogeneity, and myositis-specific autoantibody subtype.Annals of the rheumatic diseases · 2025Article
- Polyphenol blend enhances zootechnical performance, improves meat quality, and reduces the severity of wooden breast in broiler chickens.Frontiers in veterinary science · 2025Article
- Identification of copper death-associated molecular clusters and immunological profiles for lumbar disc herniation based on the machine learning.Scientific reports · 2024Article
- Therapeutics Targeting Skeletal Muscle in Amyotrophic Lateral Sclerosis.Biomolecules · 2024Review
- Effect of HY7602 Fermented Deer Antler on Physical Fatigue and Antioxidant Activity in Mice.International journal of molecular sciences · 2024Article
- Ghost messages: cell death signals spread.Cell communication and signaling : CCS · 2023Review
- TNF-α Suppresses Apelin Receptor Expression in Mouse Quadriceps Femoris-Derived Cells.Current issues in molecular biology · 2022Article
- Neutrophil and natural killer cell imbalances prevent muscle stem cell-mediated regeneration following murine volumetric muscle loss.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Therapeutic Benefit of Galectin-1: Beyond Membrane Repair, a Multifaceted Approach to LGMD2B.Cells · 2021Article
- Hindlimb Immobilization Increases IL-1β and Cdkn2a Expression in Skeletal Muscle Fibro-Adipogenic Progenitor Cells: A Link Between Senescence and Muscle Disuse Atrophy.Frontiers in cell and developmental biology · 2021Article
- eATP/P2X7R Axis: An Orchestrated Pathway Triggering Inflammasome Activation in Muscle Diseases.International journal of molecular sciences · 2020Review
- Article
- HGF-MET Signaling Shifts M1 Macrophages Toward an M2-Like Phenotype Through PI3K-Mediated Induction of Arginase-1 Expression.Frontiers in immunology · 2020Article
- Adipose Tissue-Derived Stromal Cells in Matrigel Impacts the Regeneration of Severely Damaged Skeletal Muscles.International journal of molecular sciences · 2019Article
- Fibroadipogenic progenitors are responsible for muscle loss in limb girdle muscular dystrophy 2B.Nature communications · 2019Article
- Elevated leptin levels induce inflammation through IL-6 in skeletal muscle of aged female rats.BMC musculoskeletal disorders · 2019Article
- Immunobiology of Inherited Muscular Dystrophies.Comprehensive Physiology · 2018Review
- Potent pro-inflammatory and pro-fibrotic molecules, osteopontin and galectin-3, are not major disease modulators of laminin α2 chain-deficient muscular dystrophy.Scientific reports · 2017Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundLoss-of-function mutations in the dysferlin gene (DYSF) result in a family of muscle disorders known collectively as the dysferlinopathies. Dysferlin-deficient muscle is characterized by inflammatory foci and macrophage infiltration with subsequent decline in muscle function. Whereas macrophages function to remove necrotic tissue in acute injury, their prevalence in chronic myopathy is thought to inhibit resolution of muscle regeneration. Two major classes of macrophages, classical (M1) and alternative (M2a), play distinct roles during the acute injury process. However, their individual roles in chronic myopathy remain unclear and were explored in this study.
methodsTo test the roles of the two macrophage phenotypes on regeneration in dysferlin-deficient muscle, we developed an in vitro co-culture model of macrophages and muscle cells. We assayed the co-cultures using ELISA and cytokine arrays to identify secreted factors and performed transcriptome analysis of molecular networks induced in the myoblasts.
resultsDysferlin-deficient muscle contained an excess of M1 macrophage markers, compared with WT, and regenerated poorly in response to toxin injury. Co-culturing macrophages with muscle cells showed that M1 macrophages inhibit muscle regeneration whereas M2a macrophages promote it, especially in dysferlin-deficient muscle cells. Examination of soluble factors released in the co-cultures and transcriptome analysis implicated two soluble factors in mediating the effects: IL-1β and IL-4, which during acute injury are secreted from M1 and M2a macrophages, respectively. To test the roles of these two factors in dysferlin-deficient muscle, myoblasts were treated with IL-4, which improved muscle differentiation, or IL-1β, which inhibited it. Importantly, blockade of IL-1β signaling significantly improved differentiation of dysferlin-deficient cells.
conclusionsWe propose that the inhibitory effects of M1 macrophages on myogenesis are mediated by IL-1β signals and suppression of the M1-mediated immune response may improve muscle regeneration in dysferlin deficiency. Our studies identify a potential therapeutic approach to promote muscle regeneration in dystrophic muscle.
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