scholarly journals Differential Muscle Hypertrophy Is Associated with Satellite Cell Numbers and Akt Pathway Activation Following Activin Type IIB Receptor Inhibition in Mtm1 p.R69C Mice

2014 ◽  
Vol 184 (6) ◽  
pp. 1831-1842 ◽  
Author(s):  
Michael W. Lawlor ◽  
Marissa G. Viola ◽  
Hui Meng ◽  
Rachel V. Edelstein ◽  
Fujun Liu ◽  
...  
2008 ◽  
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pp. 58-68 ◽  
Author(s):  
Abraham Jacob ◽  
Tina X. Lee ◽  
Brian A. Neff ◽  
Shyra Miller ◽  
Bradley Welling ◽  
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PLoS ONE ◽  
2011 ◽  
Vol 6 (3) ◽  
pp. e17517 ◽  
Author(s):  
Elzbieta Stankiewicz ◽  
David M. Prowse ◽  
Mansum Ng ◽  
Jack Cuzick ◽  
David Mesher ◽  
...  

2018 ◽  
Vol 9 (2) ◽  
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Qiong Wu ◽  
Jin-xian Chen ◽  
Yu Chen ◽  
Li-li Cai ◽  
Xiao-zhong Wang ◽  
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Development ◽  
2017 ◽  
Vol 144 (8) ◽  
pp. 1363-1365 ◽  
Author(s):  
John J. McCarthy ◽  
Esther E. Dupont-Versteegden ◽  
Christopher S. Fry ◽  
Kevin A. Murach ◽  
Charlotte A. Peterson

2018 ◽  
Vol 314 (5) ◽  
pp. R741-R751 ◽  
Author(s):  
Nobuki Moriya ◽  
Mitsunori Miyazaki

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.


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