Growth factors in skeletal muscle regeneration

Husmann, Irène; Soulet, Laurent; Gautron, J; Martelly, Isabelle; Barritault, Denis

doi:10.1016/s1359-6101(96)00029-9

Cited by 244 publications

(191 citation statements)

References 91 publications

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“…In vivo, the differentiation process is tightly regulated by serum growth factors and by autocrine and paracrine factors. The C2C12 cell line is sensitive to bFGF, a growth factor known to regulate satellite cell function (20,21). We show that bFGF is a more potent activator of p42/p44 MAPK compared with IGF-1 and this activation represses myogenesis.…”

mentioning

confidence: 76%

Critical Proliferation-independent Window for Basic Fibroblast Growth Factor Repression of Myogenesis via the p42/p44 MAPK Signaling Pathway

Tortorella¹,

Milasincic

Pilch

2001

Journal of Biological Chemistry

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In many cell types including myoblasts, growth factors control proliferation and differentiation, in part, via the mitogen-activated protein kinase (MAPK) pathway (also known as the extracellular regulated kinase (Erk) pathway). In C2C12 myoblast cells, insulin-like growth factor-1 and basic fibroblast growth factor (bFGF) activate MAPK/Erk, and both growth factors promote myoblast proliferation. However, these factors have opposing roles with respect to differentiation; insulin-like growth factor-1 enhances muscle cell differentiation, whereas bFGF inhibits the expression of the muscle-specific transcription factors MyoD and myogenin. Cells treated with bFGF and PD98059, a specific inhibitor of the MAPK pathway, show enhanced expression of the muscle-specific transcription factors MyoD and myogenin as compared with cells not exposed to this inhibitor. Inhibiting MAPK activity also enhances myoblast fusion and the expression of the late differentiation marker myosin heavy chain. Basic FGF mediated repression of muscle-specific genes does not result from continued cell proliferation, since bFGF-treated cells progress through only one round of cell division. We have identified a critical boundary 16 to 20 h after plating during which bFGF induced MAPK activity is able to repress myogenic gene expression and differentiation. Thus, the targets of MAPK that regulate myogenesis are functional at this time and their identification is in progress.The mitogen-activated protein kinase (MAPK) 1 signaling cascade has been implicated in the regulation of numerous cellular processes including cell growth and differentiation. The activation of the MAPK pathway occurs through ligandinduced activation of receptor tyrosine kinases that results in receptor dimerization and autophosphorylation (1). The resulting phosphotyrosine residues of the activated receptors associate with various downstream targets. For MAPK or Erk activation, in general, receptor phosphorylation leads to the binding of Grb2/SOS and activation of Ras, which in turn activates the kinase cascade consisting of Raf, its target MEK1/2 (MAP/Erk kinase), followed by MAPK activation. Activated MEK1/2 phosphorylates Thr 183 and Tyr 185 of p42/p44 MAPK rendering the kinase active such that it phosphorylates cytoplasmic and nuclear substrates (reviewed in Refs. 2-4). MAPK is strongly activated by many mitogens, suggesting these kinases may play an important role in cell proliferation, and by inference, a negative role in differentiation for appropriate cell types. Somewhat paradoxically, however, the sustained activation of MAPK's appears to be necessary for the differentiation and neurite outgrowth process in the PC12 neuronal cell line (5-9). Microinjection of constitutively active MAPK into PC12 cells results in their differentiation (8). Also, co-injection of MAPK with the dual-specificity phosphatase MAP kinase phosphatase-1, or the expression of dominant negative MAPK inhibits neuronal cell differentiation (8). On the other hand, MAPK activity antagonizes the abil...

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mentioning

confidence: 76%

Critical Proliferation-independent Window for Basic Fibroblast Growth Factor Repression of Myogenesis via the p42/p44 MAPK Signaling Pathway

Tortorella¹,

Milasincic

Pilch

2001

Journal of Biological Chemistry

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“…The secreted form ADAM12-S can cleave insulin-like growth factor (IGF)-binding protein-3 and -5 Shi et al, 2000), and in so doing promotes bioactivity of IGF-1 and -2, two positive regulators of muscle growth, survival, and regeneration (Husmann et al, 1996;Kaliman et al, 1996;Kronqvist et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

ADAM12 and α₉β₁Integrin Are Instrumental in Human Myogenic Cell Differentiation

Lafuste

Sonnet

Chazaud

et al. 2005

MBoC

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Knowledge on molecular systems involved in myogenic precursor cell (mpc) fusion into myotubes is fragmentary. Previous studies have implicated the a disintegrin and metalloproteinase (ADAM) family in most mammalian cell fusion processes. ADAM12 is likely involved in fusion of murine mpc and human rhabdomyosarcoma cells, but it requires yet unknown molecular partners to launch myogenic cell fusion. ADAM12 was shown able to mediate cell-to-cell attachment through binding ␣ 9 ␤ 1 integrin. We report that normal human mpc express both ADAM12 and ␣ 9 ␤ 1 integrin during their differentiation. Expression of ␣ 9 parallels that of ADAM12 and culminates at time of fusion. ␣ 9 and ADAM12 coimmunoprecipitate and participate to mpc adhesion. Inhibition of ADAM12/␣ 9 ␤ 1 integrin interplay, by either ADAM12 antisense oligonucleotides or blocking antibody to ␣ 9 ␤ 1 , inhibited overall mpc fusion by 47-48%, with combination of both strategies increasing inhibition up to 62%. By contrast with blockade of vascular cell adhesion molecule-1/␣ 4 ␤ 1 , which also reduced fusion, exposure to ADAM12 antisense oligonucleotides or anti-␣ 9 ␤ 1 antibody did not induce detachment of mpc from extracellular matrix, suggesting specific involvement of ADAM12-␣ 9 ␤ 1 interaction in the fusion process. Evaluation of the fusion rate with regard to the size of myotubes showed that both ADAM12 antisense oligonucleotides and ␣ 9 ␤ 1 blockade inhibited more importantly formation of large (>5 nuclei) myotubes than that of small (2-4 nuclei) myotubes. We conclude that both ADAM12 and ␣ 9 ␤ 1 integrin are expressed during postnatal human myogenic differentiation and that their interaction is mainly operative in nascent myotube growth. INTRODUCTIONAdult skeletal muscle regeneration after injury results from activation, proliferation, and fusion of mononucleated myogenic precursor cells (mpc) (Hawke and Garry, 2001). The mpc fusion results from an ordered sequence of events, including clustering and alignment of cells, establishment of close cell-to-cell contacts, and plasma membrane merging (Doberstein et al., 1997;Taylor, 2003). Various membrane proteins have been implicated in myotube formation, including N-and M-cadherins, neural cell adhesion molecule (NCAM), and vascular cell adhesion molecule (VCAM), ␣ 4 ␤ 1 and other integrins, and a disintegrin and metalloproteinases (ADAMs) (Abmayr et al., 2003). ADAMs form a family of Ͼ30 transmembrane glycoproteins with a unique domain organization, including a prodomain, a proteolytic domain (metalloprotease), an adhesion integrin-binding site formed by both disintegrin and cysteine-rich domains, an epidermal growth factor-like domain, a transmembrane domain, and a signaling cytoplasmic tail (Huovila et al., 1996;Primakoff and Myles, 2002;White, 2003). In addition, some ADAMs contain a hydrophobic sequence in a cysteine-rich region that may represent a fusion peptide, suggesting that this subclass of ADAMs might participate to plasma membrane merging (Huovila et al., 1996). Some ADAMs have been implicated i...

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“…The insulin-like growth factors IGF-I and IGF-II have dual effects on skeletal muscle differentiation in the mouse: they both stimulate the proliferation of satellite cells and promote their differentiation (Husmann et al, 1996). The primary actions of IGFs are mediated through binding and activation of their cell surface receptors.…”

Section: Genes Expressed Only During Early Myoblast Differentiation Cmentioning

confidence: 99%

Genome‐wide examination of myoblast cell cycle withdrawal during differentiation

Shen

Collier

Hlaing

et al. 2002

Developmental Dynamics

107

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Skeletal and cardiac myocytes cease division within weeks of birth. Although skeletal muscle retains limited capacity for regeneration through recruitment of satellite cells, resident populations of adult myocardial stem cells have not been identified. Because cell cycle withdrawal accompanies myocyte differentiation, we hypothesized that C2C12 cells, a mouse myoblast cell line previously used to characterize myocyte differentiation, also would provide a model for studying cell cycle withdrawal during differentiation. C2C12 cells were differentiated in culture medium containing horse serum and harvested at various time points to characterize the expression profiles of known cell cycle and myogenic regulatory factors by immunoblot analysis. BrdU incorporation decreased dramatically in confluent cultures 48 hr after addition of horse serum, as cells started to form myotubes. This finding was preceded by up-regulation of MyoD, followed by myogenin, and activation of Bcl-2. Cyclin D1 was expressed in proliferating cultures and became undetectable in cultures containing 40% fused myotubes, as levels of p21 WAF1/Cip1 increased and ␣-actin became detectable. Because C2C12 myoblasts withdraw from the cell cycle during myocyte differentiation following a course that recapitulates this process in vivo, we performed a genome-wide screen to identify other gene products involved in this process. Using microarrays containing ϳ10,000 minimally redundant mouse sequences that map to the UniGene database of the National Center for Biotechnology Information, we compared gene expression profiles between proliferating, differentiating, and differentiated C2C12 cells and verified candidate genes demonstrating differential expression by RT-PCR. Cluster analysis of differentially expressed genes revealed groups of gene products involved in cell cycle withdrawal, muscle differentiation, and apoptosis. In addition, we identified several genes, including DDAH2 and Ly-6A, whose expression specifically was up-regulated during cell cycle withdrawal coincident with early myoblast differentiation. Developmental Dynamics 226:128 -138, 2003.

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Growth factors in skeletal muscle regeneration

Cited by 244 publications

References 91 publications

Critical Proliferation-independent Window for Basic Fibroblast Growth Factor Repression of Myogenesis via the p42/p44 MAPK Signaling Pathway

Critical Proliferation-independent Window for Basic Fibroblast Growth Factor Repression of Myogenesis via the p42/p44 MAPK Signaling Pathway

ADAM12 and α₉β₁Integrin Are Instrumental in Human Myogenic Cell Differentiation

Genome‐wide examination of myoblast cell cycle withdrawal during differentiation

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Growth factors in skeletal muscle regeneration

Cited by 244 publications

References 91 publications

Critical Proliferation-independent Window for Basic Fibroblast Growth Factor Repression of Myogenesis via the p42/p44 MAPK Signaling Pathway

Critical Proliferation-independent Window for Basic Fibroblast Growth Factor Repression of Myogenesis via the p42/p44 MAPK Signaling Pathway

ADAM12 and α9β1Integrin Are Instrumental in Human Myogenic Cell Differentiation

Genome‐wide examination of myoblast cell cycle withdrawal during differentiation

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ADAM12 and α₉β₁Integrin Are Instrumental in Human Myogenic Cell Differentiation