Expression of myostatin pro domain results in muscular transgenic mice

Yang, Jinzeng; Ratovitski, Tamara; Brady, John Paul; Solomon, M.B.; Wells, Kevin D.; Wall, Robert J.

doi:10.1002/mrd.1097

Cited by 164 publications

(120 citation statements)

References 35 publications

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“…A disruption of myostatin function by transgenic expression of its propetide (the 5 0 region, 866 nucleotides) was reported to result in significant muscle growth (Yang et al, 2001). Nevertheless, the expression of myostatin mRNA did not seem to be influenced by rpGH administration in growing pigs (Ji et al, 1998), which is supported by our result that shows no significant difference in myostatin mRNA abundance between control and rpGH-treated pigs.…”

Section: Discussionsupporting

confidence: 81%

Muscle type-specific responses of myoD and calpain 3 expression to recombinant porcine growth hormone in the pig

Yang

Chen

et al. 2007

Animal

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Sixteen castrated male Large White 3 Landrace pigs were employed to investigate the muscle type-specific changes of gene expression in response to recombinant porcine growth hormone (rpGH) administration. Pigs were injected intramuscularly with rpGH (4 mg/day, n 5 8) or saline (n 5 8) for 28 days. Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to determine the mRNA abundance of genes related to muscle growth in longissimus dorsi (LD) and semitendinosus (ST) muscles. Myofibre-type composition was characterised by the ratio of the expression of myosin heavy chain (MyHC) 1, 2a or 2b relative to 2x. The results showed that the relative myofibre-type composition of neither LD nor ST was affected by rpGH administration. rpGH administration did not induce significant changes in the abundances of myostatin and myogenin mRNA in both types of muscle. MyoD and calpain 3 mRNA were significantly increased after rpGH treatment in ST muscle, whereas the difference was not significant in LD muscle. A tendency of down-regulation was observed for PGC-1a mRNA expression in ST muscle of rpGH-treated group (P 5 0.16). These results suggest that myoD, calpain 3 and probably PGC-1a may be involved in the mechanism of exogenous GH action on skeletal muscle growth; rpGH up-regulates mRNA expression of myoD and calpain 3 in a muscle type-specific manner, being more remarkable in ST than in LD, whereas no influences of rpGH on the mRNA expression of myostatin and myogenin were detected.

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Section: Discussionsupporting

confidence: 81%

Muscle type-specific responses of myoD and calpain 3 expression to recombinant porcine growth hormone in the pig

Yang

Chen

et al. 2007

Animal

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“…Similarly, mrf4 expression (4C) is higher in mstn Ϫ/Ϫ than control animals. Control animals show no mrf4 expression at day 2 after injury (22). In contrast, mstn Ϫ/Ϫ animals have substantial expression of mrf4 by day 2 after injury and beyond.…”

Section: Resultsmentioning

confidence: 95%

Muscle regeneration in the prolonged absence of myostatin

Wagner

Liu

Chang

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

176

123

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Myostatin is an endogenous inhibitor of muscle conserved across diverse species. In the absence of myostatin, there is massive muscle growth in mice, cattle, and humans. Previous studies in the mdx mouse model of muscular dystrophy demonstrate that inhibiting myostatin attenuates several features of dystrophic muscle. These findings have encouraged the development of human therapies to block myostatin. However, little is known of the long-term effects on muscle of myostatin blockade. To evaluate potential sequelae from the prolonged absence of myostatin, senescent myostatin null (mstn ؊/؊ ) mice were studied. Senescent mstn ؊/؊ mice continue to have normal muscle with increased mass and strength relative to controls. Muscles of senescent mstn ؊/؊ mice regenerate robustly from both chronic and acute injury. Early markers of regeneration are enhanced in the absence of myostatin, suggesting a mechanism for the attenuation of dystrophic features found in mdx mice lacking myostatin.aging ͉ muscular dystrophy

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“…Disruption of Mstn functionality results in increased muscle mass, decreased adiposity and improved efficiency (McPherron and Szabo et al, 1998;Yang et al, 2001;McPherron and Lee, 2002;Mitchell and Wall, 2007). Mstn null mice often exhibit muscle weights 1.5 to 2 times greater than their wild-type counterparts , whereas weights of individual fat pads are reduced (McPherron and Lee, 2002).…”

Section: Discussionmentioning

confidence: 99%

The myostatin null mutation and clenbuterol administration elicit additive effects in mice

Dilger

Gabriel

Kutzler

et al. 2010

Animal

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In mice, the myostatin (Mstn) null mutation and treatment with clenbuterol both increase muscle growth and decrease fat mass. Our objective was to determine whether mechanistic overlap exists by administering clenbuterol to Mstn null mice. Male Mstn null and wild-type mice of similar genetic backgrounds received either 0 (control) or 20 p.p.m. clenbuterol in tap water free choice for 14 days. Several traits were measured to estimate muscle and fat growth. The Mstn null mutation resulted in increased body and empty carcass weight, increased muscle weights and decreased fat pad weights. Fat content was reduced and protein content was increased in the empty carcasses of Mstn null mice. Similarly, treatment with clenbuterol resulted in increased body and empty carcass weight, increased muscle weights and reduced fat pad weights. Fat content of empty carcasses and viscera was reduced and protein content of empty carcasses was increased with clenbuterol treatment. A significant interaction of genotype and clenbuterol treatment would indicate an altered responsiveness of Mstn null mice to clenbuterol. However, only the weight of gastrocnemius muscles exhibited a significant (P 5 0.01) interaction of genotype and clenbuterol treatment, indicating that Mstn null mice were less responsive to clenbuterol compared with wild-type mice. Thus, for all other traits, the impact of Mstn null mutation and clenbuterol treatment was completely additive. These data suggest that disruption of Mstn function does not alter the response of mice to b-adrenergic agonists.

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Expression of myostatin pro domain results in muscular transgenic mice

Cited by 164 publications

References 35 publications

Muscle type-specific responses of myoD and calpain 3 expression to recombinant porcine growth hormone in the pig

Muscle type-specific responses of myoD and calpain 3 expression to recombinant porcine growth hormone in the pig

Muscle regeneration in the prolonged absence of myostatin

The myostatin null mutation and clenbuterol administration elicit additive effects in mice

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