Regulation of Myoblast Motility and Fusion by the CXCR4-associated Sialomucin, CD164

Bae, Gyu‐Un; Gaio, Ursula; Yang, Youngoo; Lee, Hyejin; Kang, Jong‐Sun; Krauss, Robert M.

doi:10.1074/jbc.m706730200

Cited by 70 publications

(50 citation statements)

References 46 publications

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“…For instance, interleukin-4 (IL-4) regulates myoblast recruitment and late-stage fusion to allow growth of myotubes/myofibers (Horsley et al, 2003). The chemokine Cxcl12 also regulates myoblast migration and myocyte fusion (Bae et al, 2008;Chong et al, 2007;Griffin et al, 2010;Melchionna et al, 2010). IL-6 promotes myogenic differentiation possibly by modulating the transcriptional program at the initiation of differentiation (BaezaRaja and Muñoz-Cánoves, 2004;Okazaki et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Flt3L is a novel regulator of skeletal myogenesis

Waldemer

Nalluri

et al. 2013

Journal of Cell Science

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SummaryVarious cues initiate multiple signaling pathways to regulate the highly coordinated process of skeletal myogenesis. Myoblast differentiation comprises a series of ordered events starting with cell cycle withdrawal and ending with myocyte fusion, with each step probably controlled by multiple extracellular signals and intracellular signaling pathways. Here we report the identification of Fms-like tyrokine kinase 3 ligand (Flt3L) signaling as a novel regulator of skeletal myogenesis. Flt3L is a multifunctional cytokine in immune cells, but its involvement in skeletal muscle formation has not been reported. We found that Flt3L is expressed in C2C12 myoblasts, with levels increasing throughout differentiation. Knockdown of Flt3L, or its receptor Flt3, suppresses myoblast differentiation, which is rescued by recombinant Flt3L or Flt3, respectively. Differentiation is not rescued, however, by recombinant ligand when the receptor is knocked down, or vice versa, suggesting that Flt3L and Flt3 function together. Flt3L knockdown also inhibits differentiation in mouse primary myoblasts. Both Flt3L and Flt3 are highly expressed in nascent myofibers during muscle regeneration in vivo, and Flt3L siRNA impairs muscle regeneration, validating the physiological significance of Flt3L function in myogenesis. We have identified a cellular mechanism for the myogenic function of Flt3L, as we show that Flt3L promotes cell cycle exit that is necessary for myogenic differentiation. Furthermore, we identify Erk as a relevant target of Flt3L signaling during myogenesis, and demonstrate that Flt3L suppresses Erk signaling through p120RasGAP. In summary, our work reveals an unexpected role for an immunoregulatory cytokine in skeletal myogenesis and a new myogenic pathway.

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Section: Discussionmentioning

confidence: 99%

Flt3L is a novel regulator of skeletal myogenesis

Waldemer

Nalluri

et al. 2013

Journal of Cell Science

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“…Its vertebrate homolog, endolyn, is targeted to endosomes and lysosomes, and functions in the maintenance of hematopoietic progenitors (Forde et al, 2007) and myoblast fusion (Bae et al, 2008). The highest degree of similarity between Vsg and Endolyn is in the transmembrane and cytoplasmic domains, including the C-terminal lysosomal sorting signals, suggesting a common underlying role for this family of sialomucins.…”

Section: Somatic Cell Ring-canal Componentsmentioning

confidence: 99%

Intercellular protein movement in syncytial Drosophila follicle cells

Airoldi¹,

McLean²,

Shimada³

et al. 2012

Development

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SummaryRing canals connecting Drosophila germline, follicle and imaginal disc cells provide direct contact of cytoplasm between cells. To date, little is known about the formation, structure, or function of the somatic ring canals present in follicle and imaginal disc cells. Here, we show by confocal and electron microscopy that Pavarotti kinesin-like protein and Visgun are stable components of somatic ring canals. Using live-cell confocal microscopy, we show that somatic ring canals form from the stabilization of mitotic cleavage furrows. In contrast to germline cells, syncytial follicle cells do not divide synchronously, are not maximally branched and their ring canals do not increase in size during egg chamber development. We show for the first time that somatic ring canals permit exchange of cytoplasmic proteins between follicle cells. These results provide insight into the composition and function of ring canals in somatic cells, implying a broader functional significance for syncytial organization of cells outside the germline.

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“…In vitro studies demonstrate that migration is a key process during myogenesis. Migration is crucial to achieve cellcell adhesion, which is necessary for differentiation (Kang et al, 2004), as well as formation and growth of myotubes in vitro (Bae et al, 2008;Jansen and Pavlath, 2006;Mylona et al, 2006;O'Connor et al, 2007). Identification of molecules that regulate cell migration might reveal potential molecular targets for improving muscle regeneration and the efficiency of celltransplantation therapies (Galvez et al, 2006;Hill et al, 2006;Palumbo et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Chemokine expression and control of muscle cell migration during myogenesis

Griffin

Apponi

Long

et al. 2010

Journal of Cell Science

134

105

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SummaryAdult regenerative myogenesis is vital for restoring normal tissue structure after muscle injury. Muscle regeneration is dependent on progenitor satellite cells, which proliferate in response to injury, and their progeny differentiate and undergo cell-cell fusion to form regenerating myofibers. Myogenic progenitor cells must be precisely regulated and positioned for proper cell fusion to occur. Chemokines are secreted proteins that share both leukocyte chemoattractant and cytokine-like behavior and affect the physiology of a number of cell types. We investigated the steady-state mRNA levels of 84 chemokines, chemokine receptors and signaling molecules, to obtain a comprehensive view of chemokine expression by muscle cells during myogenesis in vitro. A large number of chemokines and chemokine receptors were expressed by primary mouse muscle cells, especially during times of extensive cell-cell fusion. Furthermore, muscle cells exhibited different migratory behavior throughout myogenesis in vitro. One receptor-ligand pair, CXCR4-SDF-1 (CXCL12), regulated migration of both proliferating and terminally differentiated muscle cells, and was necessary for proper fusion of muscle cells. Given the large number of chemokines and chemokine receptors directly expressed by muscle cells, these proteins might have a greater role in myogenesis than previously appreciated.

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Regulation of Myoblast Motility and Fusion by the CXCR4-associated Sialomucin, CD164

Cited by 70 publications

References 46 publications

Flt3L is a novel regulator of skeletal myogenesis

Flt3L is a novel regulator of skeletal myogenesis

Intercellular protein movement in syncytial Drosophila follicle cells

Chemokine expression and control of muscle cell migration during myogenesis

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