Signaling satellite-cell activation in skeletal muscle: Markers, models, stretch, and potential alternate pathways

2005 ◽  
Vol 31 (3) ◽  
pp. 283-300 ◽  
Author(s):  
Ashley C. Wozniak ◽  
Jiming Kong ◽  
Erika Bock ◽  
Orest Pilipowicz ◽  
Judy E. Anderson
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Cell Activation ◽  
Satellite Cell Activation

scholarly journals Castration induces satellite cell activation that contributes to skeletal muscle maintenance

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

scholarly journals Satellite cell activation and apoptosis in skeletal muscle from severely burned children

2016 ◽  
Vol 594 (18) ◽  
pp. 5223-5236 ◽  
Author(s):  
Christopher S. Fry ◽  
Craig Porter ◽  
Labros S. Sidossis ◽  
Christopher Nieten ◽  
Paul T. Reidy ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Cell Activation ◽  
Satellite Cell Activation

scholarly journals Inducible Activation of Akt Increases Skeletal Muscle Mass and Force Without Satellite Cell Activation

2010 ◽  
Vol 98 (3) ◽  
pp. 153a ◽  
Author(s):  
Bert Blaauw ◽  
Canato Marta ◽  
Lisa Agatea ◽  
Luana Toniolo ◽  
Cristina Mammucari ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Cell Activation ◽  
Satellite Cell Activation ◽  
Inducible Activation

Functional and morphological improvement of skeletal muscle in Pompe disease after forced satellite cell activation

2017 ◽  
Vol 27 ◽  
pp. S161
Author(s):  
G. Schaaf ◽  
T. van Gestel ◽  
S. in ‘t Groen ◽  
A. van der Ploeg ◽  
W. Pijnappel
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Pompe Disease ◽  
Cell Activation ◽  
Satellite Cell Activation

Calcium influx through a possible coupling of cation channels impacts skeletal muscle satellite cell activation in response to mechanical stretch

2012 ◽  
Vol 302 (12) ◽  
pp. C1741-C1750 ◽  
Author(s):  
Minako Hara ◽  
Kuniko Tabata ◽  
Takahiro Suzuki ◽  
Mai-Khoi Q. Do ◽  
Wataru Mizunoya ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Calcium Ions ◽  
Calcium Ion ◽  
Cell Activation ◽  
Primary Cultures ◽  
Specific Inhibitor ◽  
Cyclic Stretch ◽  
Myogenic Stem Cells ◽  
Satellite Cell Activation

When skeletal muscle is stretched or injured, satellite cells, resident myogenic stem cells positioned beneath the basal lamina of mature muscle fibers, are activated to enter the cell cycle. This signaling pathway is a cascade of events including calcium-calmodulin formation, nitric oxide (NO) radical production by NO synthase, matrix metalloproteinase activation, release of hepatocyte growth factor (HGF) from the extracellular matrix, and presentation of HGF to the receptor c-met, as demonstrated by assays of primary cultures and in vivo experiments. Here, we add evidence that two ion channels, the mechanosensitive cation channel (MS channel) and the long-lasting-type voltage-gated calcium-ion channel (L-VGC channel), mediate the influx of extracellular calcium ions in response to cyclic stretch in satellite cell cultures. When applied to 1-h stretch cultures with individual inhibitors for MS and L-VGC channels (GsMTx-4 and nifedipine, respectively) or with a less specific inhibitor (gadolinium chloride, Gd), satellite cell activation and upstream HGF release were abolished, as revealed by bromodeoxyuridine-incorporation assays and Western blotting of conditioned media, respectively. The inhibition was dose dependent with a maximum at 0.1 μM (GsMTx-4), 10 μM (nifedipine), or 100 μM (Gd) and canceled by addition of HGF to the culture media; a potent inhibitor for transient-type VGC channels (NNC55–0396, 100 μM) did not show any significant inhibitory effect. The stretch response was also abolished when calcium-chelator EGTA (1.8 mM) was added to the medium, indicating the significance of extracellular free calcium ions in our present activation model. Finally, cation/calcium channel dependencies were further documented by calcium-imaging analyses on stretched cells; results clearly demonstrated that calcium ion influx was abolished by GsMTx-4, nifedipine, and EGTA. Therefore, these results provide an additional insight that calcium ions may flow in through L-VGC channels by possible coupling with adjacent MS channel gating that promotes the local depolarization of cell membranes to initiate the satellite cell activation cascade.

scholarly journals Hyperbaric-oxygen Reduces Inflammation And Regenerates Rats Skeletal Muscle Via Macrophage And Satellite Cell Activation.

2018 ◽  
Vol 50 (5S) ◽  
pp. 113
Author(s):  
Takuya Oyaizu ◽  
Mitsuhiro Enomoto ◽  
Naoki Yamamoto ◽  
Masaki Horie ◽  
Atsushi Okawa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Hyperbaric Oxygen ◽  
Cell Activation ◽  
Satellite Cell Activation

A role for calcium-calmodulin in regulating nitric oxide production during skeletal muscle satellite cell activation

2009 ◽  
Vol 296 (4) ◽  
pp. C922-C929 ◽  
Author(s):  
Ryuichi Tatsumi ◽  
Adam L. Wuollet ◽  
Kuniko Tabata ◽  
Shotaro Nishimura ◽  
Shoji Tabata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Methyl Ester ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Cell Activation ◽  
Calcium Ionophore ◽  
Ester Hydrochloride ◽  
Methyl Ester Hydrochloride ◽  
Satellite Cell Activation

When skeletal muscle is stretched or injured, myogenic satellite cells are activated to enter the cell cycle. This process depends on nitric oxide (NO) production by NO synthase (NOS), matrix metalloproteinase activation, release of hepatocyte growth factor (HGF) from the extracellular matrix, and presentation of HGF to the c-met receptor as demonstrated by a primary culture and in vivo assays. We now add evidence that calcium-calmodulin is involved in the satellite cell activation cascade in vitro. Conditioned medium from cultures that were treated with a calcium ionophore (A23187, ionomycin) for 2 h activated cultured satellite cells and contained active HGF, similar to the effect of mechanical stretch or NO donor treatments. The response was abolished by addition of calmodulin inhibitors (calmidazolium, W-13, W-12) or a NOS inhibitor NG-nitro-l-arginine methyl ester hydrochloride but not by its less inactive enantiomer NG-nitro-d-arginine methyl ester hydrochloride. Satellite cells were also shown to express functional calmodulin protein having a calcium-binding activity at 12 h postplating, which is the time at which the calcium ionophore was added in this study and the stretch treatment was applied in our previous experiments. Therefore, results from these experiments provide an additional insight that calcium-calmodulin mediates HGF release from the matrix and that this step in the activation pathway is upstream from NO synthesis.

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