ED2+ Macrophages Increase Selectively Myoblast Proliferation in Muscle Cultures

Massimino, Maria Lina; Rapizzi, Elena; Cantini, Marcello; Libera, Luciano Dalla; Mazzoleni, Francesco; Arslan, Paola; Carraro, Ugo

doi:10.1006/bbrc.1997.6823

Cited by 126 publications

(89 citation statements)

References 32 publications

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“…Notably, macrophages secrete both signals such as TNF-a that worsen muscle wasting via activation of the FOXO transcription factor (66, 67) and molecules that have an opposite function, such as IGF-1, a central regulator of muscle regeneration (7,56,57), or IL-10 (59, 68, 69). The activation of distinct pathways in muscle cells depending on macrophage activation leading to growth or differentiation had been described and characterized in elegant earlier studies (12,(70)(71)(72)(73)(74)(75)(76)(77).…”

Section: Discussionmentioning

confidence: 99%

Transplanted Mesoangioblasts Require Macrophage IL-10 for Survival in a Mouse Model of Muscle Injury

Bosurgi

Corna

Vezzoli

et al. 2012

The Journal of Immunology

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The aim of this study was to verify whether macrophages influence the fate of transplanted mesoangioblasts—vessel-associated myogenic precursors—in a model of sterile toxin-induced skeletal muscle injury. We have observed that in the absence of macrophages, transplanted mesoangioblasts do not yield novel fibers. Macrophages retrieved from skeletal muscles at various times after injury display features that resemble those of immunoregulatory macrophages. Indeed, they secrete IL-10 and express CD206 and CD163 membrane receptors and high amounts of arginase I. We have reconstituted the muscle-associated macrophage population by injecting polarized macrophages before mesoangioblast injection: alternatively activated, immunoregulatory macrophages only support mesoangioblast survival and function. This action depends on the secretion of IL-10 in the tissue. Our results reveal an unanticipated role for tissue macrophages in mesoangioblast function. Consequently, the treatment of muscle disorders with mesoangioblasts should take into consideration coexisting inflammatory pathways, whose activation may prove crucial for its success.

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Section: Discussionmentioning

confidence: 99%

Transplanted Mesoangioblasts Require Macrophage IL-10 for Survival in a Mouse Model of Muscle Injury

Bosurgi

Corna

Vezzoli

et al. 2012

The Journal of Immunology

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“…Factors released by cells of the monocyte/macrophage lineage can promote satellite cell proliferation in vitro (12,62). Furthermore, conditioned media from J774 macrophage cultures increased MyoD expression in myoblasts but also increased myogenin expression when applied to cultured muscle cells later in differentiation (13), indicating that macrophages could promote both proliferation and differentiation of muscle cells.…”

Section: Changes In Myeloid Cell Phenotype In Muscle Following Injurymentioning

confidence: 99%

Regulatory interactions between muscle and the immune system during muscle regeneration

Tidball

Villalta

2010

American Journal of Physiology-Regulatory, Integrative and Comp

888

987

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Tidball JG, Villalta SA. Regulatory interactions between muscle and the immune system during muscle regeneration. Am J Physiol Regul Integr Comp Physiol 298: R1173-R1187, 2010. First published March 10, 2010 doi:10.1152/ajpregu.00735.2009.-Recent discoveries reveal complex interactions between skeletal muscle and the immune system that regulate muscle regeneration. In this review, we evaluate evidence that indicates that the response of myeloid cells to muscle injury promotes muscle regeneration and growth. Acute perturbations of muscle activate a sequence of interactions between muscle and inflammatory cells. The initial inflammatory response is a characteristic Th1 inflammatory response, first dominated by neutrophils and subsequently by CD68 ϩ M1 macrophages. M1 macrophages can propagate the Th1 response by releasing proinflammatory cytokines and cause further tissue damage through the release of nitric oxide. Myeloid cells in the early Th1 response stimulate the proliferative phase of myogenesis through mechanisms mediated by TNF-␣ and IL-6; experimental prolongation of their presence is associated with delayed transition to the early differentiation stage of myogenesis. Subsequent invasion by CD163ϩ /CD206 ϩ M2 macrophages attenuates M1 populations through the release of anti-inflammatory cytokines, including IL-10. M2 macrophages play a major role in promoting growth and regeneration; their absence greatly slows muscle growth following injury or modified use and inhibits muscle differentiation and regeneration. Chronic muscle injury leads to profiles of macrophage invasion and function that differ from acute injuries. For example, mdx muscular dystrophy yields invasion of muscle by M1 macrophages, but their early invasion is accompanied by a subpopulation of M2a macrophages. M2a macrophages are IL-4 receptor ϩ /CD206 ϩ cells that reduce cytotoxicity of M1 macrophages. Subsequent invasion of dystrophic muscle by M2c macrophages is associated with progression of the regenerative phase in pathophysiology. Together, these findings show that transitions in macrophage phenotype are an essential component of muscle regeneration in vivo following acute or chronic muscle damage. skeletal muscle; macrophage; neutrophil; muscular dystrophy; chemokines SKELETAL MUSCLE HAS A REMARKABLE capacity for repair, even following severe damage. Experimental findings show that crushing muscle, killing muscle by the injection of toxins, mechanical destruction caused by large, lengthening stretches, or killing muscle fibers by freezing can be followed by the successful regeneration of muscle that leads to recovery of normal structure and function. The regenerative capacity of skeletal muscle relies largely on the presence of a population of mononucleated, myogenic cells, called satellite cells, that retain their ability to proliferate and then differentiate to either fuse with existing fibers or with other myogenic cells to generate new fibers. Thus, perturbations to the processes that normally regulate the activation, proliferat...

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“…MP-derived soluble factors inducing mpc proliferation have long been reported (Cantini et al, 1994;Cantini and Carraro, 1995;Massimino et al, 1997), and the literature on myogenic cell growth factors is extensive (reviewed by Hawke and Garry, 2001). By contrast, the significance of direct contacts between MPs and mpcs has not been previously explored in the setting of muscle regeneration.…”

Section: Introductionmentioning

confidence: 99%

Human macrophages rescue myoblasts and myotubes from apoptosis through a set of adhesion molecular systems

Sonnet

Lafuste

Arnold

et al. 2006

Journal of Cell Science

137

104

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The mechanisms underlying stromal cell supportive functions are incompletely understood but probably implicate a mixture of cytokines, matrix components and cell adhesion molecules. Skeletal muscle uses recruited macrophages to support post-injury regeneration. We and others have previously shown that macrophages secrete mitogenic factors for myogenic cells. Here, we focused on macrophage-elicited survival signals. We demonstrated that: (1) macrophage influx is temporally correlated with the disappearance of TUNEL-positive apoptotic myogenic cells during post-injury muscle regeneration in mice; (2) direct cell-cell contacts between human macrophages and myogenic cells rescue myogenic cells from apoptosis, as assessed by decreased annexin V labelling and caspase-3 activity, and by increased DIOC-6 staining, Bcl-2 expression and phosphorylation of Akt and ERK1/2 survival pathways; (3) four pro-survival cell-cell adhesion molecular systems detected by DNA macroarray are expressed by macrophages and myogenic cells in vitro and in vivo - VCAM-1-VLA-4, ICAM-1-LFA-1, PECAM-1-PECAM-1 and CX3CL1-CX3CR1; (4) macrophages deliver anti-apoptotic signals through all four adhesion systems, as assessed by functional analyses with blocking antibodies; and (5) macrophages more strongly rescue differentiated myotubes, which must achieve adhesion-induced stabilisation of their structure to survive. Macrophages could secure these cells until they establish final association with the matrix.

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ED2+ Macrophages Increase Selectively Myoblast Proliferation in Muscle Cultures

Cited by 126 publications

References 32 publications

Transplanted Mesoangioblasts Require Macrophage IL-10 for Survival in a Mouse Model of Muscle Injury

Transplanted Mesoangioblasts Require Macrophage IL-10 for Survival in a Mouse Model of Muscle Injury

Regulatory interactions between muscle and the immune system during muscle regeneration

Human macrophages rescue myoblasts and myotubes from apoptosis through a set of adhesion molecular systems

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