Effect of myostatin on turkey myogenic satellite cells and embryonic myoblasts

McFarland, Douglas C.; Velleman, Sandra G.; Pesall, Jane E.; Liu, Caini

doi:10.1016/j.cbpa.2006.04.020

Cited by 43 publications

(22 citation statements)

References 26 publications

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“…These findings were confirmed in separate experiments in which H9c2 cardiomyocytes were transfected with a Mst cDNA expression constructs which revealed that Mst inhibits G1 to S phase progression. These data on Mst effects on cardiomyocytes are analogous to those reported in cultures of skeletal myoblasts in which Mst also has been shown to inhibit cell replication, mainly by interfering with the progression into S phase of the cell cycle (Artaza et al 2002, McCroskery et al 2003, Sakuma et al 2004, Shyu et al 2005, McFarland et al 2006, Tsao et al 2006. Our results with the H9c2 cell line also coincide with a very recent study (McKoy et al 2007) in primary rat embryonic cardiomyocytes showing that Mst is expressed faintly in these cells, and that recombinant Mst inhibits cell proliferation via upregulation of p21 and Smad2 phosphorylation, thus blocking the G1 to S phase progression.…”

Section: Discussionsupporting

confidence: 78%

Alterations in myostatin expression are associated with changes in cardiac left ventricular mass but not ejection fraction in the mouse

Artaza

Reisz‐Porszasz

Dow

et al. 2007

Journal of Endocrinology

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Myostatin (Mst) is a negative regulator of skeletal muscle in humans and animals. It is moderately expressed in the heart of sheep and cattle, increasing considerably after infarction. Genetic blockade of Mst expression increases cardiomyocyte growth. We determined whether Mst overexpression in the heart of transgenic mice reduces left ventricular size and function, and inhibits in vitro cardiomyocyte proliferation. Young transgenic mice overexpressing Mst in the heart (Mst transgenic mice (TG) under a muscle creatine kinase (MCK) promoter active in cardiac and skeletal muscle, and Mst knockout (Mst (K/K)) mice were used. Xiscan angiography revealed that the left ventricular ejection fraction did not differ between the Mst TG and the Mst (K/K) mice, when compared with their respective wild-type strains, despite the decrease in whole heart and left ventricular size in Mst TG mice, and their increase in Mst (K/K) animals. The expected changes in cardiac Mst were measured by RT-PCR and western blot. Mst and its receptor (ActRIIb) were detected by RT-PCR in rat H9c2 cardiomyocytes. Transfection of H9c2 with plasmids expressing Mst under muscle-specific creatine kinase promoter, or cytomegalovirus promoter, enhanced p21 and reduced cdk2 expression, when assessed by western blot. A decrease in cell number occurred by incubation with recombinant Mst (formazan assay), without affecting apoptosis or cardiomyocyte size. Anti-Mst antibody increased cardiomyocyte replication, whereas transfection with the Mst-expressing plasmids inhibited it. In conclusion, Mst does not affect cardiac systolic function in mice overexpressing or lacking the active protein, but it reduces cardiac mass and cardiomyocyte proliferation.

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Section: Discussionsupporting

confidence: 78%

Alterations in myostatin expression are associated with changes in cardiac left ventricular mass but not ejection fraction in the mouse

Artaza

Reisz‐Porszasz

Dow

et al. 2007

Journal of Endocrinology

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“…5). Previous studies indicate that myostatin is important in maintaining MPC quiescence (McCroskery et al 2003; McFarland et al 2006; McFarlane et al 2008) and may explain the apparently high expression levels in day 1 MPCs. Several reports have described the potential for myostatin to being sequestered to the cell membrane via proteogylcans, like decorin, and this mechanism may be responsible for local functional regulation (Miura et al 2006; Nishimura et al 2007; Zhu et al 2007; Kishioka et al 2008).…”

Section: Discussionmentioning

confidence: 95%

In vitro indeterminate teleost myogenesis appears to be dependent on Pax3

Froehlich

Galt

Charging

et al. 2013

In Vitro Cell.Dev.Biol.-Animal

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The zebrafish (Danio rerio) has been used extensively as a model system for developmental studies but, unlike most teleost fish, it grows in a determinate-like manner. A close relative, the giant danio (Devario cf. aequipinnatus), grows indeterminately, displaying both hyperplasia and hypertrophy of skeletal myofibers as an adult. To better understand adult muscle hyperplasia, a postlarval/postnatal process that closely resembles secondary myogenesis during development, we characterized the expression of Pax3/7, c-Met, syndecan-4, Myf5, MyoD1, myogenin, and myostatin during in vitro myogenesis, a technique that allows for the complete progression of myogenic precursor cells to myotubes. Pax7 appears to be expressed only in newly activated MPCs while Pax3 is expressed through most of the myogenic program, as are c-Met and syndecan-4. MyoD1 appears important in all stages of myogenesis, while Myf5 is likely expressed at low to background levels, and myogenin expression is enriched in myotubes. Myostatin, like MyoD1, appears to be ubiquitous at all stages. This is the first comprehensive report of key myogenic factor expression patterns in an indeterminate teleost, one that strongly suggests that Pax3 and/or Myf5 may be involved in the regulation of this paradigm. Further, it validates this species as a model organism for studying adult myogenesis in vitro, especially mechanisms underlying nascent myofiber recruitment.

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“…Mstn −/− muscle contains more satellite cells per unit myofiber domain and the satellite cells are more resistance to activation, suggesting that Mstn maintains satellite cells in a quiescent state [14,15]. In addition, Mstn also inhibits the proliferation of satellite cells derived from several animal species [16,17,18,19]. By contrast, Mstn seems to promote the differentiation of myoblasts in fish [20].…”

Section: Introductionmentioning

confidence: 99%

Myostatin facilitates slow and inhibits fast myosin heavy chain expression during myogenic differentiation

Wang

Kim

et al. 2012

Biochemical and Biophysical Research Communications

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Skeletal muscles in the limb and body trunk are composed of heterogeneous myofibers expressing different isoforms of myosin heavy chain (Myh), including type I (slow, Myh7), IIA (intermediate, Myh2), IIX (fast, Myh1) and IIB (very fast, Myh4). While the contraction force and speed of a muscle are known to be determined by the relative abundance of myofibers expressing each Myh isoform, it is unclear how specific combinations of myofiber types are formed and regulated at the cellular and molecular level. We report here that myostatin (Mstn) positively regulates slow but negatively regulates fast Myh isoforms. Mstn was expressed at higher levels in the fast muscle myoblasts and myofibers than in the slow muscle counterparts. Interestingly, Mstn knockout led to a shift of Myh towards faster isoforms, suggesting an inhibitory role of Mstn in fast Myh expression. Consistently, when induced to differentiate, Mstn null myoblasts formed myotubes preferentially expressing fast Myh. Conversely, treatment of myoblasts with a recombinant Mstn protein upregulated Myh7 but downregulated Myh4 gene expression in newly formed myotubes. Importantly, both Mstn antibody and soluble activin type 2B receptor inhibited slow Myh7 and promoted fast Myh4 expression, indicating that myostatin acts through canonical activin receptor to regulate the expression of Myh genes. These results demonstrate a role of myostatin in the specification of myofiber types during myogenic differentiation.

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Effect of myostatin on turkey myogenic satellite cells and embryonic myoblasts

Cited by 43 publications

References 26 publications

Alterations in myostatin expression are associated with changes in cardiac left ventricular mass but not ejection fraction in the mouse

Alterations in myostatin expression are associated with changes in cardiac left ventricular mass but not ejection fraction in the mouse

In vitro indeterminate teleost myogenesis appears to be dependent on Pax3

Myostatin facilitates slow and inhibits fast myosin heavy chain expression during myogenic differentiation

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