Inflammatory monocytes recruited after skeletal muscle injury switch into antiinflammatory macrophages to support myogenesis
Ludovic Arnold,Adeline Henry,Françoise Poron,Yasmine Baba-Amer,Nico van Rooijen,Anne Plonquet,Romain K. Gherardi,Bénédicte Chazaud +7 more
TL;DR: In conclusion, injured skeletal muscle recruits monocyte (MO) exhibiting inflammatory profiles that operate phagocytosis and rapidly convert to antiinflammatory MPs that stimulate myogenesis and fiber growth.
read more
Abstract: Macrophages (MPs) are important for skeletal muscle regeneration in vivo and may exert beneficial effects on myogenic cell growth through mitogenic and antiapoptotic activities in vitro. However, MPs are highly versatile and may exert various, and even opposite, functions depending on their activation state. We studied monocyte (MO)/MP phenotypes and functions during skeletal muscle repair. Selective labeling of circulating MOs by latex beads in CX3CR1GFP/+ mice showed that injured muscle recruited only CX3CR1lo/Ly-6C+ MOs from blood that exhibited a nondividing, F4/80lo, proinflammatory profile. Then, within muscle, these cells switched their phenotype to become proliferating antiinflammatory CX3CR1hi/Ly-6C− cells that further differentiated into F4/80hi MPs. In vitro, phagocytosis of muscle cell debris induced a switch of proinflammatory MPs toward an antiinflammatory phenotype releasing transforming growth factor β1. In co-cultures, inflammatory MPs stimulated myogenic cell proliferation, whereas antiinflammatory MPs exhibited differentiating activity, assessed by both myogenin expression and fusion into myotubes. Finally, depletion of circulating MOs in CD11b–diphtheria toxin receptor mice at the time of injury totally prevented muscle regeneration, whereas depletion of intramuscular F4/80hi MPs at later stages reduced the diameter of regenerating fibers. In conclusion, injured skeletal muscle recruits MOs exhibiting inflammatory profiles that operate phagocytosis and rapidly convert to antiinflammatory MPs that stimulate myogenesis and fiber growth.
read more
Chat with Paper
AI Agents for this Paper
Find similar papers on Google Scholar, PubMed and Arxiv
Write a critical review of this paper
Analyze citations of this paper to find unaddressed research gaps
Citations
Immune Cell Trafficking to the Liver.
TL;DR: This work reviews pathways and interactions that underlies the pathophysiology of autoimmune liver diseases, nonalcoholic steatohepatitis, and liver transplantation, and potential targets that have been identified to be exploited for therapeutic purposes.
39
Methacrylic acid-based hydrogels enhance skeletal muscle regeneration after volumetric muscle loss in mice.
TL;DR: In this article, the regenerative effects of two biomaterials (MAA-poly(ethylene glycol) and MAA-collagen) were investigated to treat VML injuries in murine tibialis anterior muscles.
39
Signaling pathways in macrophages: molecular mechanisms and therapeutic targets.
Ming Li,Mengjie Wang,Yuanjia Wen,Hongfei Zhang,Guang-Nian Zhao,Qinglei Gao +5 more
TL;DR: An overview of the basic physiology of macrophages and the regulatory pathways within them is provided and directions for further research on therapeutic strategies targeting macrophage signaling pathways, which are promising to improve the efficacy of disease treatment are provided.
39
Technical Advance: Monitoring the trafficking of neutrophil granulocytes and monocytes during the course of tissue inflammation by noninvasive 19F MRI
Sebastian Temme,Christoph Jacoby,Zhaoping Ding,Florian Bönner,Nadine Borg,Jürgen Schrader,Ulrich Flögel +6 more
TL;DR: 19F MRI, in combination with the matrigel/LPS model, permits the noninvasive analysis of neutrophil and monocyte infiltration over the complete course of inflammation in vivo.
39
Long-Term Evaluation of Functional Outcomes Following Rat Volumetric Muscle Loss Injury and Repair.
Ellen L. Mintz,Juliana A. Passipieri,Isabelle R Franklin,Victoria M Toscano,Emma C Afferton,Poonam Sharma,George J. Christ +6 more
TL;DR: The importance of "tuning" the application of tissue engineering technology platforms to the specific requirements of diverse VML injuries in order to improve functional outcomes is emphasized.
39
References
Alternative activation of macrophages
TL;DR: The evidence in favour of alternative macrophage activation by the TH2-type cytokines interleukin-4 (IL-4) and IL-13 is assessed, and its limits and relevance to a range of immune and inflammatory conditions are defined.
6.4K
Monocyte and macrophage heterogeneity
Siamon Gordon,Philip R. Taylor +1 more
TL;DR: Recent studies have shown that monocyte heterogeneity is conserved in humans and mice, allowing dissection of its functional relevance: the different monocyte subsets seem to reflect developmental stages with distinct physiological roles, such as recruitment to inflammatory lesions or entry to normal tissues.
5.4K
Obesity induces a phenotypic switch in adipose tissue macrophage polarization
TL;DR: Diet-induced obesity leads to a shift in the activation state of ATMs from an M2-polarized state in lean animals that may protect adipocytes from inflammation to an M1 proinflammatory state that contributes to insulin resistance.
The peroxisome proliferator-activated receptor-gamma is a negative regulator of macrophage activation
Mercedes Ricote,Andrew C. Li,Andrew C. Li,Timothy M. Willson,Carolyn J. Kelly,Christopher K. Glass +5 more
TL;DR: It is shown that PPAR-γ is markedly upregulated in activated macrophages and inhibits the expression of the inducible nitric oxide synthase, gelatinase B and scavenger receptor A genes in response to 15d-PGJ2 and synthetic PPar-γ ligands, suggesting that PPARS and locally produced prostaglandin D2 metabolites are involved in the regulation of inflammatory responses.
3.7K
Blood Monocytes Consist of Two Principal Subsets with Distinct Migratory Properties
TL;DR: Using a murine adoptive transfer system to probe monocyte homing and differentiation in vivo, two functional subsets among murine blood monocytes are identified: a short-lived CX(3)CR1(lo)CCR2(+)Gr1(+) subset that is actively recruited to inflamed tissues and a CX (3) CR1(hi)CCS1-dependent recruitment to noninflamed tissues.
3.5K