Satellite cell addition is/is not obligatory for skeletal muscle hypertrophy

2007 ◽  
Vol 103 (3) ◽  
pp. 1104-1106 ◽  
Author(s):  
Charlotte Rehfeldt
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy

scholarly journals Akt1 deficiency diminishes skeletal muscle hypertrophy by reducing satellite cell proliferation

2018 ◽  
Vol 314 (5) ◽  
pp. R741-R751 ◽  
Author(s):  
Nobuki Moriya ◽  
Mitsunori Miyazaki
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Protein Synthesis ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Satellite Cells ◽  
Muscle Hypertrophy ◽  
Mtor Signaling ◽  
Skeletal Muscle Hypertrophy ◽  
Satellite Cell Proliferation

Skeletal muscle mass is determined by the net dynamic balance between protein synthesis and degradation. Although the Akt/mechanistic target of rapamycin (mTOR)-dependent pathway plays an important role in promoting protein synthesis and subsequent skeletal muscle hypertrophy, the precise molecular regulation of mTOR activity by the upstream protein kinase Akt is largely unknown. In addition, the activation of satellite cells has been indicated as a key regulator of muscle mass. However, the requirement of satellite cells for load-induced skeletal muscle hypertrophy is still under intense debate. In this study, female germline Akt1 knockout (KO) mice were used to examine whether Akt1 deficiency attenuates load-induced skeletal muscle hypertrophy through suppressing mTOR-dependent signaling and satellite cell proliferation. Akt1 KO mice showed a blunted hypertrophic response of skeletal muscle, with a diminished rate of satellite cell proliferation following mechanical overload. In contrast, Akt1 deficiency did not affect the load-induced activation of mTOR signaling and the subsequent enhanced rate of protein synthesis in skeletal muscle. These observations suggest that the load-induced activation of mTOR signaling occurs independently of Akt1 regulation and that Akt1 plays a critical role in regulating satellite cell proliferation during load-induced muscle hypertrophy.

scholarly journals Interleukin-6 Is an Essential Regulator of Satellite Cell-Mediated Skeletal Muscle Hypertrophy

2008 ◽  
Vol 7 (1) ◽  
pp. 33-44 ◽  
Author(s):  
Antonio L. Serrano ◽  
Bernat Baeza-Raja ◽  
Eusebio Perdiguero ◽  
Mercè Jardí ◽  
Pura Muñoz-Cánoves
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Interleukin 6 ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy

β2-Integrins contribute to skeletal muscle hypertrophy in mice

2008 ◽  
Vol 295 (4) ◽  
pp. C1026-C1036 ◽  
Author(s):  
Joseph S. Marino ◽  
Brian J. Tausch ◽  
Christopher L. Dearth ◽  
Marc V. Manacci ◽  
Thomas J. McLoughlin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Hypertrophy ◽  
Muscle Differentiation ◽  
Normal Function ◽  
Total Protein Content ◽  
Wild Type ◽  
Skeletal Muscle Hypertrophy ◽  
Myoblast Proliferation

We tested the contribution of β2-integrins, which are important for normal function of neutrophils and macrophages, to skeletal muscle hypertrophy after mechanical loading. Using the synergist ablation model of hypertrophy and mice deficient in the common β-subunit of β2-integrins (CD18−/−), we found that overloaded muscles of wild-type mice had greater myofiber size, dry muscle mass, and total protein content compared with CD18−/−mice. The hypertrophy in wild-type mice was preceded by elevations in neutrophils, macrophages, satellite cell/myoblast proliferation (5′-bromo-2′-deoxyuridine- and desmin-positive cells), markers of muscle differentiation (MyoD1 and myogenin gene expression and formation and size of regenerating myofibers), signaling for protein synthesis [phosphorylation of Akt and 70-kDa ribosomal protein S6 kinase (p70S6k)], and reduced signaling for protein degradation (decreased gene expression of muscle atrophy F box/atrogin-1). The deficiency in β2-integrins, however, altered the accumulation profile of neutrophils and macrophages, disrupted the temporal profile of satellite cell/myoblast proliferation, reduced the markers of muscle differentiation, and impaired the p70S6k signaling, all of which could serve as mechanisms for the impaired hypertrophy in overloaded CD18−/−mice. In conclusion, our findings indicate that β2-integrins contribute to the hypertrophic response to muscle overload by temporally regulating satellite cells/myoblast proliferation and by enhancing muscle differentiation and p70S6k signaling.

scholarly journals Robust Skeletal Muscle Hypertrophy in Satellite Cell Depleted Muscle

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
John Joseph McCarthy ◽  
Jyothi Mula ◽  
Mitsunori Miyazaki ◽  
Esther Dupont‐Versteegden ◽  
Charles Keller ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy

scholarly journals Srf-Dependent Paracrine Signals Produced by Myofibers Control Satellite Cell-Mediated Skeletal Muscle Hypertrophy

2012 ◽  
Vol 15 (1) ◽  
pp. 25-37 ◽  
Author(s):  
Aline Guerci ◽  
Charlotte Lahoute ◽  
Sophie Hébrard ◽  
Laura Collard ◽  
Dany Graindorge ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy

scholarly journals Resident muscle stem cells are not required for testosterone-induced skeletal muscle hypertrophy

2019 ◽  
Vol 317 (4) ◽  
pp. C719-C724 ◽  
Author(s):  
Davis A. Englund ◽  
Bailey D. Peck ◽  
Kevin A. Murach ◽  
Ally C. Neal ◽  
Hannah A. Caldwell ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Satellite Cell ◽  
Muscle Fiber ◽  
Muscle Hypertrophy ◽  
Cross Sectional ◽  
Muscle Stem Cells ◽  
Cell Abundance ◽  
Skeletal Muscle Hypertrophy ◽  
Testosterone Administration

It is postulated that testosterone-induced skeletal muscle hypertrophy is driven by myonuclear accretion as the result of satellite cell fusion. To directly test this hypothesis, we utilized the Pax7-DTA mouse model to deplete satellite cells in skeletal muscle followed by testosterone administration. Pax7-DTA mice (6 mo of age) were treated for 5 days with either vehicle [satellite cell replete (SC+)] or tamoxifen [satellite cell depleted (SC-)]. Following a washout period, a testosterone propionate or sham pellet was implanted for 21 days. Testosterone administration caused a significant increase in muscle fiber cross-sectional area in SC+ and SC- mice in both oxidative (soleus) and glycolytic (plantaris and extensor digitorum longus) muscles. In SC+ mice treated with testosterone, there was a significant increase in both satellite cell abundance and myonuclei that was completely absent in testosterone-treated SC- mice. These findings provide direct evidence that testosterone-induced muscle fiber hypertrophy does not require an increase in satellite cell abundance or myonuclear accretion. Listen to a podcast about this Rapid Report with senior author E. E. Dupont-Versteegden ( https://ajpcell.podbean.com/e/podcast-on-paper-that-shows-testosterone-induced-skeletal-muscle-hypertrophy-does-not-need-muscle-stem-cells /).

Last Word on Point:Counterpoint: Satellite cell addition is/is not obligatory for skeletal muscle hypertrophy

2007 ◽  
Vol 103 (3) ◽  
pp. 1107-1107 ◽  
Author(s):  
Roddy S. O'Connor ◽  
Grace K. Pavlath ◽  
J. J. McCarthy ◽  
K. A. Esser
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy
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