Chemokine expression and control of muscle cell migration during myogenesis

Griffin, Christine A.; Apponi, Luciano H.; Long, Kimberly; Pavlath, Grace K.

doi:10.1242/dev.058446

Cited by 31 publications

(54 citation statements)

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“…Furthermore, myoblasts cultured on various artificial substrates are also motile and migrate in response to a variety of factors, including chemokines (Corti et al, 2001;Odemis et al, 2007;Griffin et al, 2010), growth factors (Robertson et al, 1993a;Bischoff, 1997;Lee et al, 1999;Corti et al, 2001;Villena and Brandan, 2004) and other molecules (Nedachi et al, 2009;Tokura et al, 2011). Except for Cxcr4 [chemokine (C-X-C motif) receptor 4], the receptor for the chemokine Sdf1 (stromal-derived factor 1; Cxcl12 -Mouse Genome Informatics) (Griffin et al, 2010), the effect of depleting these molecules on cell fusion has not been tested. Cell motility changes greatly during differentiation, with myocytes exhibiting less motility than myoblasts (Powell, 1973;Griffin et al, 2010) and becoming unresponsive to several potent Box 2.…”

Section: Myoblast Migration Recognition and Adhesion In Micementioning

confidence: 99%

“…Except for Cxcr4 [chemokine (C-X-C motif) receptor 4], the receptor for the chemokine Sdf1 (stromal-derived factor 1; Cxcl12 -Mouse Genome Informatics) (Griffin et al, 2010), the effect of depleting these molecules on cell fusion has not been tested. Cell motility changes greatly during differentiation, with myocytes exhibiting less motility than myoblasts (Powell, 1973;Griffin et al, 2010) and becoming unresponsive to several potent Box 2. Experimental systems for studying myoblast fusion: strengths and limitations Drosophila Strengths • Genetically tractable system with a rapid generation time.…”

Section: Myoblast Migration Recognition and Adhesion In Micementioning

confidence: 99%

“…inducers of myoblast migration, such as hepatocyte growth factor (Hgf) and platelet-derived growth factor (Pdgf) (Griffin et al, 2010). This decrease in motility would increase the probability of cell-cell contact, thereby triggering differentiation (Krauss et al, 2005) and allowing myocytes to fuse with one another and with nascent myotubes (Nowak et al, 2009).…”

Section: Myoblast Migration Recognition and Adhesion In Micementioning

confidence: 99%

“…This decrease in motility would increase the probability of cell-cell contact, thereby triggering differentiation (Krauss et al, 2005) and allowing myocytes to fuse with one another and with nascent myotubes (Nowak et al, 2009). As myotubes begin to form, muscle cells preferentially move into some fields and out of others (Chazaud et al, 1998), suggesting that migration is directed in response to chemotactic factors secreted by muscle cells (Bondesen et al, 2007;Griffin et al, 2010).…”

Section: Myoblast Migration Recognition and Adhesion In Micementioning

confidence: 99%

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Myoblast fusion: lessons from flies and mice

2012

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The fusion of myoblasts into multinucleate syncytia plays a fundamental role in muscle function, as it supports the formation of extended sarcomeric arrays, or myofibrils, within a large volume of cytoplasm. Principles learned from the study of myoblast fusion not only enhance our understanding of myogenesis, but also contribute to our perspectives on membrane fusion and cell-cell fusion in a wide array of model organisms and experimental systems. Recent studies have advanced our views of the cell biological processes and crucial proteins that drive myoblast fusion. Here, we provide an overview of myoblast fusion in three model systems that have contributed much to our understanding of these events: the Drosophila embryo; developing and regenerating mouse muscle; and cultured rodent muscle cells. IntroductionThe process of fusing two adjacent membranes accomplishes many goals that are crucial to the development and maintenance of living organisms. Broadly, membrane fusion can occur intracellularly, as with synaptic vesicles, or between cells, as for sperm-egg fusion. Cell fusion occurs in a broad range of organisms, including Saccharomyces cerevisiae and Caenorhabditis elegans, and between several cell types, such as macrophages, placental trophoblasts and myoblasts. Experimental analysis of fusion in these systems has revealed the involvement of a diverse array of specialized molecules.Myoblast fusion, a fundamental step in the differentiation of muscle in most organisms, can involve tens of thousands of myoblasts, Given the complexity of the musculature, fusion must be a regulated process in which the appropriate number of cells fuse at the appropriate time and place. Often these cells migrate long distances prior to fusion, and fusion can involve multiple cell types, necessitating cell recognition and adhesion, which are crucial to accurate and efficient fusion. In addition to the early fusion events that occur during embryogenesis, vertebrate muscle tissue is able to regenerate in response to damage and disease. This regeneration involves proliferation of muscle satellite cells (see Glossary, Box 1) and their subsequent fusion to repair the damaged muscles. The focus of this review is the process of myoblast fusion, which involves cell migration, adhesion and signaling transduction pathways leading up to the actual fusion event. We review the crucial role of the actin cytoskeleton and actin polymerizing proteins, and recently revealed membrane protrusions that may drive fusion itself. We describe three powerful systems for this analysis: Drosophila embryogenesis; mouse embryogenesis and regeneration; and rodent tissue culture. We highlight the genes and morphological events involved in myoblast fusion, as revealed by each system. With the emergence of Danio rerio as another model for myoblast fusion, we also list relevant homologs in this system (Tables 1, 2). Experimental systems for the analysis of myoblast fusionThe ability to isolate and propagate mammalian myoblasts that could differentiate and fuse in...

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Section: Myoblast Migration Recognition and Adhesion In Micementioning

confidence: 99%

Section: Myoblast Migration Recognition and Adhesion In Micementioning

confidence: 99%

Section: Myoblast Migration Recognition and Adhesion In Micementioning

confidence: 99%

Section: Myoblast Migration Recognition and Adhesion In Micementioning

confidence: 99%

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Myoblast fusion: lessons from flies and mice

2012

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“…Griffin i wsp. (23) wykazali, że CXCR4 ulega ekspresji zarówno w pierwotnych mysich mioblastach, jak i miocytach, a jego ligand SDF-1α zwiększa migrację obu typów komórek. Ponadto, utrata CXCR4 prowadziła do zahamowania różnicowania, o czym świadczyła zmniejszona ekspresja swoistych białek mięśniowych, takich jak miogenina i ciężki łańcuch miozyny.…”

Section: Rola Chemokin W Regulacji Miogenezyunclassified

Role of proinflammatory cytokines and growth factors in skeletal muscle regeneration

Milewska¹,

Grzelkowska-Kowalczyk²

2016

Medycyna Weterynaryjna

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Podstawowymi funkcjami mięśni szkieletowych są: zapewnienie lokomocji i ruchów oddechowych, zachowanie postawy, wytwarzanie ciepła oraz udział w utrzymaniu homeostazy metabolicznej. Mięśnie szkieletowe wykazują stałą zdolność do adaptacji, wywołanej przez czynniki środowiskowe i mechaniczne, zapewniającej podtrzymanie swoistych funkcji i masy tkanki. Regeneracja mięśni szkieletowych jest ściśle regulowana przez dynamiczne zależności pomiędzy czynnikami wewnętrznymi i zewnętrznymi, kształ-tującymi mikrośrodowisko (tzw. "niszę") komórek macierzystych obecnych w mięśniach szkieletowych. Postęp w rozwoju biologii komórki, biologii molekularnej i genetyki, który dokonał się w ostatnich latach, znacznie poszerzył wiedzę o wzroście i regeneracji mięśni szkieletowych, a badania nad niszą komórek macierzystych mięśni ujawniły wiele molekularnych mechanizmów kontrolujących wzrost masy mięśnio-wej. Przebieg miogenezy oraz rola czynników wzrostu i cytokin w rozwoju tkanki mięśniowej są identyczne u człowieka i zwierząt, stąd ich poznanie ma wymiar ogólnobiologiczny. Względna masa mięśni szkieletowych stanowi kryterium w ocenie ilości i jakości mięsa w tuszy. Wiedza o miejscowych mechanizmach kształ-tujących niszę macierzystych komórek mięśniowych pozwala wnioskować o przebiegu procesów regeneracyjnych zachodzących w mięśniach szkieletowych po urazach i zabiegach chirurgicznych.Znaczenie badań nad miogenezą w naukach weterynaryjnych i zootechnicznych Powierzchniowe położenie większości mięśni w organizmie naraża je na uszkodzenie, spowodowane przez skrajne warunki termiczne lub skaleczenia, ponadto intensywny wysiłek fizyczny powoduje bezpośrednie mechaniczne zniszczenie błony komórkowej lub całych włókien mięśniowych (59). Miogeneza regeneracyjna u dorosłych osobników jest zależna od obecnych w mięśniach komórek progenitorowych, zwanych komórkami satelitowymi (32). Urazy i intensywny wysiłek fizyczny aktywują komórki satelitowe, które podejmują proliferację, różnicowanie i fuzję z sąsiadującymi włóknami mięśniowymi, co prowadzi do regeneracji uszkodzonej tkanki lub hipertrofii mię-śni związanej z treningiem (57). Zjawiska zachodzące podczas miogenezy są ściśle kontrolowane przez szereg biologicznie aktywnych czynników działających endokrynnie lub lokalnie (auto-, parakrynnie), takich Milewska M., Grzelkowska-Kowalczyk K.Role of proinflammatory cytokines and growth factors in skeletal muscle regeneration Summary Skeletal muscle healing after injury can be divided into three distinct but overlapping phases. The destruction phase is characterized by rupture followed by necrosis of muscle fibers, formation of hematoma and inflammatory reaction. During the repair phase a necrotic tissue is phagocyted by macrophages, muscle fibers are regenerating and connective tissue scars are formed. The remodeling phase concerns the period when regenerating muscle fibers mature, scar contraction and reorganization occurs and the muscle recovers its functional efficiency. Proinflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α) and growth factors ...

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Injury and Subsequent Regeneration of Muscles for Activation of Local Innate Immunity to Facilitate the Development and Relapse of Autoimmune Myositis in C57BL/6 Mice

Kimura

Hirata

Miyasaka

et al. 2015

Arthritis & Rheumatology

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Objective. To determine whether injury and regeneration of the skeletal muscles induce an inflammatory milieu that facilitates the development and relapse of autoimmune myositis.Methods. The quadriceps of C57BL/6 mice were injured with bupivacaine hydrochloride (BPVC) and evaluated histologically. Macrophages and regenerating myofibers in the treated muscles and differentiating C2C12 myotubes were examined for cytokine expression. Mice were immunized with C protein fragments at the base of the tail and in the right hind footpads (day 0) to evoke systemic anti-C protein immunity and to induce local myositis in the right hind limbs. The contralateral quadriceps muscles were injured with BPVC or phosphate buffered saline (PBS) on day 7 or after spontaneous regression of myositis (day 42). The quadriceps muscle in nonimmunized mice was injured with BPVC on day 7. The muscles were examined histologically 14 days after treatment.Results. The BPVC-injured muscles had macrophage infiltration most abundantly at 3 days after the injection, with emergence of regenerating fibers from day 5. The macrophages expressed inflammatory cytokines, including tumor necrosis factor ␣, interleukin-1␤, and CCL2. Regenerating myofibers and C2C12 myotubes also expressed the cytokines. The BPVC-injected muscles from nonimmunized mice had regenerating myofibers with resolved cell infiltration 14 days after treatment. In mice preimmunized with C protein fragments, the muscles injected with BPVC on day 7 as well as on day 42, but not those injected with PBS, had myositis accompanied by CD8؉ T cell infiltration.Conclusion. Injury and regeneration could set up an inflammatory milieu in the muscles and facilitate the development and relapse of autoimmune myositis.Polymyositis (PM) is a chronic autoimmune disease that affects the systemic striated muscles. Histologic examination of the affected muscles revealed invasion of CD8ϩ T cells into the non-necrotic muscle fibers (1). The CD8ϩ T cells surrounding muscle fibers expressed perforins, which were located eccentrically in the vicinity of the muscle fibers (2). PM patients were found to have clonal CD8ϩ T cell expansions in the peripheral blood more frequently than healthy donors (3). These expanded clones were identified in the affected muscles. All of these clues indicate involvement of CD8ϩ cytotoxic T lymphocytes (CTLs) in the pathogenesis of PM.We developed C protein-induced myositis (CIM) as a mouse model of PM, in which cytotoxic CD8ϩ T cells are responsible for the muscle injury (4,5). Investigation of its pathologic processes re-

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Chemokine expression and control of muscle cell migration during myogenesis

Cited by 31 publications

References 1 publication

Myoblast fusion: lessons from flies and mice

Myoblast fusion: lessons from flies and mice

Role of proinflammatory cytokines and growth factors in skeletal muscle regeneration

Injury and Subsequent Regeneration of Muscles for Activation of Local Innate Immunity to Facilitate the Development and Relapse of Autoimmune Myositis in C57BL/6 Mice

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