Impaired hypertrophy in myoblasts is improved with testosterone administration

Deane, Colleen S.; Hughes, David C.; Sculthorpe, Nicholas; Lewis, Mark P.; Stewart, Claire E.; Sharples, Adam P.

doi:10.1016/j.jsbmb.2013.05.005

Cited by 35 publications

(47 citation statements)

References 75 publications

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“…Additional support for a role of PI3K was also observed in control C 2 C 12 myotubes and C 2 C 12 myotubes that were subjected to population doubling to mimic “aged” skeletal muscle. Here, inhibition of PI3K reduced the testosterone (100 nM) induced increase in myotube differentiation and diameter in both cell types (Deane, Hughes et al, 2013). Despite these findings, the relationship between activation of either AR or PI3K and mTORC1 signaling remains elusive.…”

Section: 2 Molecular Regulation Of Muscle Protein Synthesis By Andrmentioning

confidence: 92%

Androgen-mediated regulation of skeletal muscle protein balance

Rossetti

Steiner

Gordon

2017

Molecular and Cellular Endocrinology

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Androgens significantly alter muscle mass in part by shifting protein balance in favor of net protein accretion. During various atrophic conditions, the clinical impact of decreased production or bioavailability of androgens (termed hypogonadism) is important as a loss of muscle mass is intimately linked with survival outcome. While androgen replacement therapy increases muscle mass in part by restoring protein balance, this is not a comprehensive treatment option due to potential side effects. Therefore, an understanding of the mechanisms by which androgens alter protein balance is needed for the development of androgen-independent therapies. While the data in humans suggest androgens alter protein balance (both synthesis and breakdown) in the fasted metabolic state, a predominant molecular mechanism(s) behind this observation is still lacking. This failure is likely due in part to inconsistent experimental design between studies including failure to control nutrient/feeding status, the method of altering androgens, and the model systems utilized.

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Section: 2 Molecular Regulation Of Muscle Protein Synthesis By Andrmentioning

confidence: 92%

Androgen-mediated regulation of skeletal muscle protein balance

Rossetti

Steiner

Gordon

2017

Molecular and Cellular Endocrinology

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“…Second, androgen-induced stimulation of the GH/IGF1 axis leads to the activation of the anabolic Akt-mTOR pathway (Basaria & Bhasin 2012, Dubois et al 2012, Deane et al 2013, Purves-Smith et al 2014. Studies regarding the effect of testosterone administration on IGF1 levels and the impact of this on muscle mass are not fully concordant, but it is generally agreed that IGF1 is important for mediating the anabolic effects of testosterone, primarily via promoting proliferation and differentiation of myoblasts, as well as influencing satellite cell activation and/or number (Chen et al 2005, Sinha-Hikim et al 2006, MacLean et al 2008, Svensson et al 2010, Ibebunjo et al 2011, Serra et al 2013b, White et al 2013.…”

Section: Stimulation Of the Gh/igf1 Axismentioning

confidence: 99%

Targeting muscle signaling pathways to minimize adverse effects of androgen deprivation

Rooy¹,

Grossmann²,

Zajac³

et al. 2015

Endocrine-Related Cancer

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Androgen deprivation therapy (ADT) is a highly effective treatment used in w30% of men with prostate cancer. Adverse effects of ADT on muscle are significant with consistent losses in muscle mass. However, effects of ADT on muscle strength and physical function, of most relevance to the patient, are less well understood. This is in part due to the fact that muscle effects of ADT at the cellular, genetic and protein level, critical to the understanding of the pathophysiology of sarcopenia, have come into focus only recently. This review highlights the complexity of androgen-dependent signaling in muscle with an emphasis on recent findings in the regulation of muscle growth and muscle atrophy pathways. Furthermore, the effects of ADT and testosterone on skeletal muscle histology, gene expression and protein transcription are discussed. A better mechanistic understanding of the regulation of muscle mass and function by androgens should not only pave the way for developing targeted promyogenic interventions for men with prostate cancer receiving ADT but also may have wider implications for age-associated sarcopenia in the general population.

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“…8,24,25 These cells showed impaired differentiation compared with parental control cells. Moreover, these cells had similar morphology and signaling properties to those observed in aged human muscle cells.…”

Section: Discussionmentioning

confidence: 93%

“…For morphology analysis, cells were fixed with methanol/acetone as described previously. 8 The cells were counted using a hemocytometer by light microscopy. Three wells were counted for each condition.…”

Section: Cell Countingmentioning

confidence: 99%

Proliferative effect of Hachimijiogan, a Japanese herbal medicine, in C2C12 skeletal muscle cells

Takeda

Tsuiji

et al. 2015

Maturitas

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Background: Hachimijiogan (HJG), Ba-Wei-Di-Huang-Wan in Chinese, is one of the most popular herbal medicines in Japanese Kampo. HJG is often prescribed for the prevention and treatment of age-related diseases. Muscle atrophy plays an important role in aging-related disabilities such as sarcopenia. The purpose of this study was to investigate the possible beneficial effect of HJG on skeletal muscle. Methods: Cells of murine skeletal muscle myoblast cell line C2C12 were used as an in vitro model of muscle cell proliferation and differentiation. The effect of HJG on C2C12 cell proliferation and differentiation was assessed. We counted the number of myotubes morphologically to assess the degree of differentiation. Results: HJG treatment (200 µg/mL) for 3 days significantly increased C2C12 cell number by 1.23-fold compared with that of the control. HJG promoted the proliferation of C2C12 cells through activation of the ERK1/2 signaling pathway without affecting the Akt signaling pathway. HJG did not affect the differentiation of C2C12 cells. Conclusion: HJG had beneficial effects on skeletal muscle myoblast proliferation. These findings may provide a useful intervention for the prevention and treatment of sarcopenia.

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Impaired hypertrophy in myoblasts is improved with testosterone administration

Cited by 35 publications

References 75 publications

Androgen-mediated regulation of skeletal muscle protein balance

Androgen-mediated regulation of skeletal muscle protein balance

Targeting muscle signaling pathways to minimize adverse effects of androgen deprivation

Proliferative effect of Hachimijiogan, a Japanese herbal medicine, in C2C12 skeletal muscle cells

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