Substrate elasticity affects bovine satellite cell activation kinetics in vitro

2013 ◽  
Vol 91 (5) ◽  
pp. 2083-2090 ◽  
Author(s):  
M. R. Lapin ◽  
J. M. Gonzalez ◽  
S. E. Johnson
Author(s):  
Alessandra Renzini ◽  
Anna Benedetti ◽  
Marina Bouché ◽  
Leopoldo Silvestroni ◽  
Sergio Adamo ◽  
...  

Single myofiber isolation protocols allow to obtain an in vitro system in which the physical association between the myofiber and its stem cells, the satellite cells, is adequately preserved. This technique is an indispensable tool by which the muscle regeneration process can be recapitulated and studied in each specific phase, from satellite cell activation to proliferation, from differentiation to fusion. This study aims to clarify the effect of different culture conditions on single myofibers, their associated satellite cells, and the physiological behavior of the satellite cells upon long term culture. By direct observations of the cultures, we compared different experimental conditions and their effect on both satellite cell behavior and myofiber viability.


2021 ◽  
Vol 2 (2) ◽  
pp. 100482
Author(s):  
Rodrigo Canibano-Fraile ◽  
Emma Boertjes ◽  
Stela Bozhilova ◽  
W.W.M. Pim Pijnappel ◽  
Gerben J. Schaaf

2000 ◽  
Vol 278 (1) ◽  
pp. C174-C181 ◽  
Author(s):  
Kristy J. Miller ◽  
Deepa Thaloor ◽  
Sarah Matteson ◽  
Grace K. Pavlath

Hepatocyte growth factor (HGF) is the only known growth factor that activates quiescent satellite cells in skeletal muscle. We hypothesized that local delivery of HGF may enhance regeneration after trauma by increasing the number of myoblasts available for restoring normal tissue architecture. Injection of HGF into muscle at the time of injury increases myoblast number but does not enhance tissue repair as determined using quantitative histological analyses. Rather, depending on the dose and the timing of HGF administration relative to the injury, regeneration can be inhibited. The greatest inhibitory effect is observed when HGF is administered on the day of injury and continued for 3 days, corresponding to the time when satellite cell activation, proliferation, and early differentiation normally occur. To establish a mechanism for this inhibition, we show that HGF can act directly on primary muscle cells to block differentiation. These results demonstrate that 1) exogenous HGF synergizes with factors in damaged muscle to increase myoblast number, 2) regeneration is not regulated solely by myoblast number, and 3) HGF inhibits muscle differentiation both in vitro and in vivo.


Author(s):  
Gerben J. Schaaf ◽  
Tom JM van Gestel ◽  
Esther Brusse ◽  
Robert M. Verdijk ◽  
Irenaeus FM de Coo ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Theodora Pavlidou ◽  
Milica Marinkovic ◽  
Marco Rosina ◽  
Claudia Fuoco ◽  
Simone Vumbaca ◽  
...  

The regeneration of the muscle tissue relies on the capacity of the satellite stem cell (SC) population to exit quiescence, divide asymmetrically, proliferate, and differentiate. In age-related muscle atrophy (sarcopenia) and several dystrophies, regeneration cannot compensate for the loss of muscle tissue. These disorders are associated with the depletion of the satellite cell pool or with the loss of satellite cell functionality. Recently, the establishment and maintenance of quiescence in satellite cells have been linked to their metabolic state. In this work, we aimed to modulate metabolism in order to preserve the satellite cell pool. We made use of metformin, a calorie restriction mimicking drug, to ask whether metformin has an effect on quiescence, proliferation, and differentiation of satellite cells. We report that satellite cells, when treated with metformin in vitro, ex vivo, or in vivo, delay activation, Pax7 downregulation, and terminal myogenic differentiation. We correlate the metformin-induced delay in satellite cell activation with the inhibition of the ribosome protein RPS6, one of the downstream effectors of the mTOR pathway. Moreover, in vivo administration of metformin induces a belated regeneration of cardiotoxin- (CTX-) damaged skeletal muscle. Interestingly, satellite cells treated with metformin immediately after isolation are smaller in size and exhibit reduced pyronin Y levels, which suggests that metformin-treated satellite cells are transcriptionally less active. Thus, our study suggests that metformin delays satellite cell activation and differentiation by favoring a quiescent, low metabolic state.


2018 ◽  
Vol 1 (1) ◽  
pp. 1-16 ◽  
Author(s):  
Alanna Klose ◽  
Wenxuan Liu ◽  
Nicole D. Paris ◽  
Sophie Forman ◽  
John J. Krolewski ◽  
...  

Stem Cells ◽  
2020 ◽  
Vol 39 (3) ◽  
pp. 331-344
Author(s):  
Alvin Wong ◽  
Steven M. Garcia ◽  
Stanley Tamaki ◽  
Katharine Striedinger ◽  
Emilie Barruet ◽  
...  

1995 ◽  
Vol 242 (3) ◽  
pp. 329-336 ◽  
Author(s):  
S. C. J. M. Jacobs ◽  
J. H. J. Wokke ◽  
P. R. Bär ◽  
A. L. Bootsma

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