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.

scholarly journals A Role for Nitric Oxide in Muscle Repair: Nitric Oxide–mediated Activation of Muscle Satellite Cells

2000 ◽  
Vol 11 (5) ◽  
pp. 1859-1874 ◽  
Author(s):  
Judy E. Anderson
Keyword(s):  
Nitric Oxide ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Knockout Mice ◽  
Cell Activation ◽  
Mdx Mice ◽  
Muscle Repair ◽  
Muscle Satellite Cells ◽  
Satellite Cell Activation

Muscle satellite cells are quiescent precursors interposed between myofibers and a sheath of external lamina. Although their activation and recruitment to cycle enable muscle repair and adaptation, the activation signal is not known. Evidence is presented that nitric oxide (NO) mediates satellite cell activation, including morphological hypertrophy and decreased adhesion in the fiber-lamina complex. Activation in vivo occurred within 1 min after injury. Cell isolation and histology showed that pharmacological inhibition of nitric oxide synthase (NOS) activity prevented the immediate injury-induced myogenic cell release and delayed the hypertrophy of satellite cells in that muscle. Transient activation of satellite cells in contralateral muscles 10 min later suggested that a circulating factor may interact with NO-mediated signaling. Interestingly, satellite cell activation in muscles of mdx dystrophic mice and NOS-I knockout mice quantitatively resembled NOS-inhibited release of normal cells, in agreement with reports of displaced and reduced NOS expression in dystrophin-deficient mdx muscle and the complete loss of NOS-I expression in knockout mice. Brief NOS inhibition in normal and mdx mice during injury produced subtle alterations in subsequent repair, including apoptosis in myotube nuclei and myotube formation inside laminar sheaths. Longer NOS inhibition delayed and restricted the extent of repair and resulted in fiber branching. A model proposes the hypothesis that NO release mediates satellite cell activation, possibly via shear-induced rapid increases in NOS activity that produce “NO transients.”

A calcineurin- and NFAT-dependent pathway regulates Myf5 gene expression in skeletal muscle reserve cells

2001 ◽  
Vol 114 (2) ◽  
pp. 303-310 ◽  
Author(s):  
B.B. Friday ◽  
G.K. Pavlath
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Satellite Cell ◽  
Cell Activation ◽  
Molecular Mechanisms ◽  
Fiber Type ◽  
Calcium Ionophore ◽  
Cell Populations ◽  
Mrna Levels ◽  
Dependent Pathway

Myf5 is a member of the muscle regulatory factor family of transcription factors and plays an important role in the determination, development, and differentiation of skeletal muscle. However, factors that regulate the expression and activity of Myf5 itself are not well understood. Recently, a role for the calcium-dependent phosphatase calcineurin was suggested in three distinct pathways in skeletal muscle: differentiation, hypertrophy, and fiber-type determination. We propose that one downstream target of calcineurin and the calcineurin substrate NFAT in skeletal muscle is regulation of Myf5 gene expression. For these studies, we used myotube cultures that contain both multinucleated myotubes and quiescent, mononucleated cells termed ‘reserve’ cells, which share many characteristics with satellite cells. Treatment of such myotube cultures with the calcium ionophore ionomycin results in an approximately 4-fold increase in Myf5 mRNA levels, but similar effects are not observed in proliferating myoblast cultures indicating that Myf5 is regulated by different pathways in different cell populations. The increase in Myf5 mRNA levels in myotube cultures requires the activity of calcineurin and NFAT, and can be specifically enhanced by overexpressing the NFATc isoform. We used immunohistochemical analyses and fractionation of the cell populations to demonstrate that the calcium regulated expression of Myf5 occurs in the mononucleated reserve cells. We conclude that Myf5 gene expression is regulated by a calcineurin- and NFAT-dependent pathway in the reserve cell population of myotube cultures. These results may provide important insights into the molecular mechanisms responsible for satellite cell activation and/or the renewal of the satellite cell pool following activation and proliferation.

scholarly journals Metformin Delays Satellite Cell Activation and Maintains Quiescence

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Theodora Pavlidou ◽  
Milica Marinkovic ◽  
Marco Rosina ◽  
Claudia Fuoco ◽  
Simone Vumbaca ◽  
...  
Keyword(s):  
Satellite Cell ◽  
Muscle Tissue ◽  
Satellite Cells ◽  
Cell Activation ◽  
Myogenic Differentiation ◽  
Metabolic State ◽  
Cell Pool ◽  
Age Related ◽  
Satellite Cell Activation

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.

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

scholarly journals Post-transcriptional regulation of satellite cell quiescence by TTP-mediated mRNA decay

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Melissa A Hausburg ◽  
Jason D Doles ◽  
Sandra L Clement ◽  
Adam B Cadwallader ◽  
Monica N Hall ◽  
...  
Keyword(s):  
Satellite Cell ◽  
Satellite Cells ◽  
Muscle Injury ◽  
Mrna Decay ◽  
Cell Activation ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Cell Quiescence ◽  
Satellite Cell Activation ◽  
Transcriptional Regulatory Mechanisms

Skeletal muscle satellite cells in their niche are quiescent and upon muscle injury, exit quiescence, proliferate to repair muscle tissue, and self-renew to replenish the satellite cell population. To understand the mechanisms involved in maintaining satellite cell quiescence, we identified gene transcripts that were differentially expressed during satellite cell activation following muscle injury. Transcripts encoding RNA binding proteins were among the most significantly changed and included the mRNA decay factor Tristetraprolin. Tristetraprolin promotes the decay of MyoD mRNA, which encodes a transcriptional regulator of myogenic commitment, via binding to the MyoD mRNA 3′ untranslated region. Upon satellite cell activation, p38α/β MAPK phosphorylates MAPKAP2 and inactivates Tristetraprolin, stabilizing MyoD mRNA. Satellite cell specific knockdown of Tristetraprolin precociously activates satellite cells in vivo, enabling MyoD accumulation, differentiation and cell fusion into myofibers. Regulation of mRNAs by Tristetraprolin appears to function as one of several critical post-transcriptional regulatory mechanisms controlling satellite cell homeostasis.

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
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