scholarly journals Methodological issues limit interpretation of negative effects of satellite cell depletion on adult muscle hypertrophy

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
Keyword(s):  
Satellite Cell ◽  
Muscle Hypertrophy ◽  
Cell Depletion ◽  
Methodological Issues ◽  
Negative Effects ◽  
Adult Muscle

scholarly journals Myonuclear transcriptional dynamics in response to exercise following satellite cell depletion

iScience ◽  
2021 ◽  
pp. 102838
Author(s):  
Yuan Wen ◽  
Davis A. Englund ◽  
Bailey D. Peck ◽  
Kevin A. Murach ◽  
John J. McCarthy ◽  
...  
Keyword(s):  
Satellite Cell ◽  
Cell Depletion ◽  
Transcriptional Dynamics ◽  
Response To Exercise

scholarly journals The influence of satellite cell‐depletion on glycosaminoglycan accumulation in aged skeletal muscle

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Zakkary James Hardyniec ◽  
Jonah D Lee ◽  
Charlotte A. Peterson
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Cell Depletion

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 Depletion of resident muscle stem cells negatively impacts running volume, physical function, and muscle fiber hypertrophy in response to lifelong physical activity

2020 ◽  
Vol 318 (6) ◽  
pp. C1178-C1188 ◽  
Author(s):  
Davis A. Englund ◽  
Kevin A. Murach ◽  
Cory M. Dungan ◽  
Vandré C. Figueiredo ◽  
Ivan J. Vechetti ◽  
...  
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Physical Function ◽  
Satellite Cell ◽  
Muscle Fiber ◽  
Satellite Cells ◽  
Cell Depletion ◽  
Muscle Adaptation ◽  
Adult Skeletal Muscle

To date, studies that have aimed to investigate the role of satellite cells during adult skeletal muscle adaptation and hypertrophy have utilized a nontranslational stimulus and/or have been performed over a relatively short time frame. Although it has been shown that satellite cell depletion throughout adulthood does not drive skeletal muscle loss in sedentary mice, it remains unknown how satellite cells participate in skeletal muscle adaptation to long-term physical activity. The current study was designed to determine whether reduced satellite cell content throughout adulthood would influence the transcriptome-wide response to physical activity and diminish the adaptive response of skeletal muscle. We administered vehicle or tamoxifen to adult Pax7-diphtheria toxin A (DTA) mice to deplete satellite cells and assigned them to sedentary or wheel-running conditions for 13 mo. Satellite cell depletion throughout adulthood reduced balance and coordination, overall running volume, and the size of muscle proprioceptors (spindle fibers). Furthermore, satellite cell participation was necessary for optimal muscle fiber hypertrophy but not adaptations in fiber type distribution in response to lifelong physical activity. Transcriptome-wide analysis of the plantaris and soleus revealed that satellite cell function is muscle type specific; satellite cell-dependent myonuclear accretion was apparent in oxidative muscles, whereas initiation of G protein-coupled receptor (GPCR) signaling in the glycolytic plantaris may require satellite cells to induce optimal adaptations to long-term physical activity. These findings suggest that satellite cells play a role in preserving physical function during aging and influence muscle adaptation during sustained periods of physical activity.

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
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