Bmp Signaling at the Tips of Skeletal Muscles Regulates the Number of Fetal Muscle Progenitors and Satellite Cells during Development

Wang, Hui; Noulet, Fanny; Edom-Vovard, Frédérique; Tozer, Samuel; Grand, Fabien Le; Duprez, Delphine

doi:10.1016/j.devcel.2010.06.002

Cited by 19 publications

(24 citation statements)

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“…Myostatinnull mice or mice in which the myostatin has been disrupted show enhanced skeletal muscle growth (Kambadur et al, 1997;McPherron et al, 1997). By contrast, a recent study reveals that over-expression of Bmp4 at the tips of chick limb skeletal muscles increases the number of fetal muscle progenitors and satellite cells, indicating that TGF superfamily members may also promote skeletal muscle development (Wang et al, 2010). Consistent with this, our study clearly shows that inactivation of Smad4 in tongue myogenic cells results in defects in myogenic…”

Section: Smad4 Is Required For Myogenic Differentiation and Myoblast supporting

confidence: 82%

A TGFβ-Smad4-Fgf6 signaling cascade controls myogenic differentiation and myoblast fusion during tongue development

et al. 2012

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The tongue is a muscular organ and plays a crucial role in speech, deglutition and taste. Despite the important physiological functions of the tongue, little is known about the regulatory mechanisms of tongue muscle development. TGFβ family members play important roles in regulating myogenesis, but the functional significance of Smad-dependent TGFβ signaling in regulating tongue skeletal muscle development remains unclear. In this study, we have investigated Smad4-mediated TGFβ signaling in the development of occipital somite-derived myogenic progenitors during tongue morphogenesis through tissue-specific inactivation of Smad4 (using Myf5-Cre;Smad4(flox/flox) mice). During the initiation of tongue development, cranial neural crest (CNC) cells occupy the tongue buds before myogenic progenitors migrate into the tongue primordium, suggesting that CNC cells play an instructive role in guiding tongue muscle development. Moreover, ablation of Smad4 results in defects in myogenic terminal differentiation and myoblast fusion. Despite compromised muscle differentiation, tendon formation appears unaffected in the tongue of Myf5-Cre;Smad4(flox/flox) mice, suggesting that the differentiation and maintenance of CNC-derived tendon cells are independent of Smad4-mediated signaling in myogenic cells in the tongue. Furthermore, loss of Smad4 results in a significant reduction in expression of several members of the FGF family, including Fgf6 and Fgfr4. Exogenous Fgf6 partially rescues the tongue myoblast fusion defect of Myf5-Cre;Smad4(flox/flox) mice. Taken together, our study demonstrates that a TGFβ-Smad4-Fgf6 signaling cascade plays a crucial role in myogenic cell fate determination and lineage progression during tongue myogenesis.

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Section: Smad4 Is Required For Myogenic Differentiation and Myoblast supporting

confidence: 82%

A TGFβ-Smad4-Fgf6 signaling cascade controls myogenic differentiation and myoblast fusion during tongue development

et al. 2012

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“…Moreover, the research performed on a mouse model showed that GDF15/MIC-1 gene plays a critical role in the central regulation of appetite and body weight (Tsai et al 2013). Other studies confirmed that equally important in the regulation of development of muscle cells are BMP proteins (Wang et al 2010). Our results indicated that in the Limousin breed both BMP4 and BMP7 genes have been affected by breeding selection focused mainly on improving meat content in a carcass.…”

Section: Discussionsupporting

confidence: 53%

“…Other studies confirmed that equally important in the regulation of development of muscle cells are BMP proteins (Wang et al . ). Our results indicated that in the Limousin breed both BMP4 and BMP7 genes have been affected by breeding selection focused mainly on improving meat content in a carcass.…”

Section: Discussionmentioning

confidence: 97%

Identification of genome‐wide selection signatures in the Limousin beef cattle breed

Gurgul

Szmatoła

Ropka‐Molik

et al. 2015

J Animal Breeding Genetics

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The study is aimed at identifying selection footprints within the genome of Limousin cattle. With the use of Extended Haplotype Homozygosity test, supplemented with correction for variation in recombination rates across the genome, we created map of selection footprints and detected 173 significant (p < 0.01) core haplotypes being potentially under positive selection. Within these regions, a number of candidate genes associated inter alia with skeletal muscle growth (GDF15, BMP7, BMP4 and TGFB3) or postmortem proteolysis and meat maturation (CAPN1 and CAPN5) were annotated. Noticeable clusters of selection footprints were detected on chromosomes 1, 4, 8 and 14, which are known to carry several quantitative trait loci for growth traits and meat quality. The study provides information about the genes and metabolic pathways potentially modified under the influence of directional selection, aimed at improving beef production characteristics in Limousin cattle.

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“…However in contrast to TGF-, BMPs then signal through Smad1/3/8, as well as other protein kinases such as p38 MAPK [287,289,332]. Studies have unveiled a role in the regulation of the numbers of foetal muscle progenitors [333] and activation of satellite cells during muscle regeneration [333][334][335][336][337]. Furthermore, BMP inhibitors, in particular Noggin and Gremlin, have also been found to be crucial for the proper differentiation of muscle progenitor cells [338][339][340].…”

Section: Bmpmentioning

confidence: 95%

Pharmacologically Targeting the Primary Defect and Downstream Pathology in Duchenne Muscular Dystrophy

Fairclough

Perkins²,

Davies³

2012

CGT

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DMD is a devastatingly progressive muscle wasting disorder of childhood that significantly shortens life expectancy. Despite efforts to develop an effective therapy that dates back over a century, clinical interventions are still restricted to management of symptoms rather than a cure. The rationale to develop effective therapies changed in 1986 with the discovery of the dystrophin gene. Since then extensive research into both the molecular basis and pathophysiology of DMD has paved the way not only for development of strategies which aim to correct the primary defect, but also towards the identification of countless therapeutic targets with the potential to alleviate the downstream pathology. In addition to gene and cell-based therapies, which aim to deliver the missing gene and/or protein, an exciting spectrum of pharmacological approaches aimed at modulating therapeutic targets within DMD muscle cells through the use of small drugs are also being developed. This review presents promising pharmacological approaches aimed at targeting the primary defect, including suppression of nonsense mutations and functional compensation by upregulation of the dystrophin homologue, utrophin. Downstream of the primary membrane fragility, inflammation and fibrosis are reduced by blocking NF-κB, TGF-α and TGF-β, and free radical damage has been targeted using antioxidants and dietary/nutritional supplements. There are new hopes that ACE and PDE5 inhibitors can protect against skeletal as well as cardiac pathology, and modulating Ca2+ influx, NO, BMP, protein degradation and the mitochondrial permeability pore hold further promise in tackling the complex pathogenesis of this multifaceted disorder.

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Bmp Signaling at the Tips of Skeletal Muscles Regulates the Number of Fetal Muscle Progenitors and Satellite Cells during Development

Cited by 19 publications

References 0 publications

A TGFβ-Smad4-Fgf6 signaling cascade controls myogenic differentiation and myoblast fusion during tongue development

A TGFβ-Smad4-Fgf6 signaling cascade controls myogenic differentiation and myoblast fusion during tongue development

Identification of genome‐wide selection signatures in the Limousin beef cattle breed

Pharmacologically Targeting the Primary Defect and Downstream Pathology in Duchenne Muscular Dystrophy

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