Estrogen influences satellite cell activation and proliferation following downhill running in rats

2008 ◽  
Vol 104 (2) ◽  
pp. 347-353 ◽  
Author(s):  
Deborah L. Enns ◽  
Peter M. Tiidus
Keyword(s):  
Satellite Cells ◽  
Cell Activation ◽  
Myogenic Differentiation ◽  
Immunohistochemical Analysis ◽  
Treadmill Running ◽  
Female Rats ◽  
Downhill Running ◽  
Glucuronidase Activity ◽  
Estrogen Exposure ◽  
Satellite Cell Activation

To investigate the influence of estrogen on postexercise muscle repair processes, we examined the effects of estrogen supplementation (0.25-mg pellet) on numbers of myofibers positive for markers of total, activated, and proliferating satellite cells in rat skeletal muscles 72 h following downhill running. Ovariectomized female rats ( n = 44) were divided into four groups ( n = 11 per group): sham (no estrogen) controls (SC); sham, exercised (SE); estrogen-supplemented controls (EC); and estrogen-supplemented, exercised (EE). After 8 days of estrogen exposure, animals were exposed to 90 min of treadmill running at 17 m/min (−13.5°). Seventy-two hours later, soleus and white vastus muscles were removed and immunostained for total [paired box homeotic gene 7 (Pax7)], [activated myogenic differentiation factor D (MyoD)], and proliferating [5-bromo-2′-deoxyuridine (BrdU)] satellite cells. β-Glucuronidase activity was increased ( P < 0.05) in both muscles following exercise; however, the postexercise elevations in enzyme activity were attenuated in the EE group compared with the SE group in the soleus ( P < 0.05). Immunohistochemical analysis revealed that exercised groups displayed increased numbers of myofibers containing total, activated, and proliferating satellite cells compared with control groups ( P < 0.05). Furthermore, greater numbers of fibers positive for markers of total, activated, and proliferating satellite cells were observed postexercise in EE animals compared with SE animals for both muscles ( P < 0.05). The results demonstrate that estrogen may potentially influence postdamage repair of skeletal muscle through activation of satellite cells.

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 Myostatin negatively regulates satellite cell activation and self-renewal

2003 ◽  
Vol 162 (6) ◽  
pp. 1135-1147 ◽  
Author(s):  
Seumas McCroskery ◽  
Mark Thomas ◽  
Linda Maxwell ◽  
Mridula Sharma ◽  
Ravi Kambadur
Keyword(s):  
Satellite Cell ◽  
Satellite Cells ◽  
Cell Activation ◽  
Unit Length ◽  
Immunohistochemical Analysis ◽  
Cell Number ◽  
Negative Regulator ◽  
Self Renewal ◽  
Satellite Cell Activation

Satellite cells are quiescent muscle stem cells that promote postnatal muscle growth and repair. Here we show that myostatin, a TGF-β member, signals satellite cell quiescence and also negatively regulates satellite cell self-renewal. BrdU labeling in vivo revealed that, among the Myostatin-deficient satellite cells, higher numbers of satellite cells are activated as compared with wild type. In contrast, addition of Myostatin to myofiber explant cultures inhibits satellite cell activation. Cell cycle analysis confirms that Myostatin up-regulated p21, a Cdk inhibitor, and decreased the levels and activity of Cdk2 protein in satellite cells. Hence, Myostatin negatively regulates the G1 to S progression and thus maintains the quiescent status of satellite cells. Immunohistochemical analysis with CD34 antibodies indicates that there is an increased number of satellite cells per unit length of freshly isolated Mstn−/− muscle fibers. Determination of proliferation rate suggests that this elevation in satellite cell number could be due to increased self-renewal and delayed expression of the differentiation gene (myogenin) in Mstn−/− adult myoblasts. Taken together, these results suggest that Myostatin is a potent negative regulator of satellite cell activation and thus signals the quiescence of satellite cells.

Exercise-induced satellite cell activation in growing and mature skeletal muscle

1987 ◽  
Vol 63 (5) ◽  
pp. 1816-1821 ◽  
Author(s):  
K. C. Darr ◽  
E. Schultz
Keyword(s):  
Satellite Cell ◽  
Cross Sections ◽  
Time Course ◽  
Cell Activation ◽  
Treadmill Running ◽  
Rapid Decline ◽  
Fiber Damage ◽  
Single Bout ◽  
Satellite Cell Activation ◽  
Exercise Induced

The time course and extent of satellite cell activation were studied in the soleus (m-SOL) and extensor digitorum longus (m-EDL) muscles of untrained growing and mature rats after a single bout of prolonged eccentric treadmill running. At 24, 48, 72, and 120 h postexercise, satellite cell mitotic activity was quantitated in autoradiographs of whole-fiber segments after injection of [3H]thymidine. Fiber damage and localization of labeled cells were also examined in muscle cross sections. Labeling in growing muscles progressively increased to peak levels (approximately 250% of control) at 72 h postexercise, whereas mature muscles exhibited an earlier peak (approximately 250% of control) at 24 (m-SOL) and 48 (m-EDL) h, followed by a more rapid decline to control levels by 120 h postexercise. In all exercised muscles the calculated satellite cell activation was far greater than required to repair the small number (less than 3.0%) of necrotic fibers identified at the light-microscopic level. These results suggest that satellite cells were activated not only on fibers exhibiting overt necrosis but also on those with lesions not discernible with light microscopy.

scholarly journals Stra13 regulates satellite cell activation by antagonizing Notch signaling

2007 ◽  
Vol 177 (4) ◽  
pp. 647-657 ◽  
Author(s):  
Hong Sun ◽  
Li Li ◽  
Cécile Vercherat ◽  
Neriman Tuba Gulbagci ◽  
Sujata Acharjee ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Cell Activation ◽  
Cellular Proliferation ◽  
Myogenic Differentiation ◽  
Critical Role ◽  
Skeletal Muscle Regeneration ◽  
Notch Activity ◽  
Satellite Cell Activation

Satellite cells play a critical role in skeletal muscle regeneration in response to injury. Notch signaling is vital for satellite cell activation and myogenic precursor cell expansion but inhibits myogenic differentiation. Thus, precise spatial and temporal regulation of Notch activity is necessary for efficient muscle regeneration. We report that the basic helix-loop-helix transcription factor Stra13 modulates Notch signaling in regenerating muscle. Upon injury, Stra13−/− mice exhibit increased cellular proliferation, elevated Notch signaling, a striking regeneration defect characterized by degenerated myotubes, increased mononuclear cells, and fibrosis. Stra13−/− primary myoblasts also exhibit enhanced Notch activity, increased proliferation, and defective differentiation. Inhibition of Notch signaling ex vivo and in vivo ameliorates the phenotype of Stra13−/− mutants. We demonstrate in vitro that Stra13 antagonizes Notch activity and reverses the Notch-imposed inhibition of myogenesis. Thus, Stra13 plays an important role in postnatal myogenesis by attenuating Notch signaling to reduce myoblast proliferation and promote myogenic differentiation.

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.

In vivo satellite cell activation via Myf5 and MyoD in regenerating mouse skeletal muscle

1999 ◽  
Vol 112 (17) ◽  
pp. 2895-2901 ◽  
Author(s):  
R.N. Cooper ◽  
S. Tajbakhsh ◽  
V. Mouly ◽  
G. Cossu ◽  
M. Buckingham ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Cell Activation ◽  
Muscle Fibres ◽  
Adult Skeletal Muscle ◽  
Satellite Cell Activation ◽  
Slow Muscle Fibres ◽  
Myogenic Factors ◽  
Beta Galactosidase

Regeneration of adult skeletal muscle is an asynchronous process requiring the activation, proliferation and fusion of satellite cells, to form new muscle fibres. This study was designed to determine the pattern of expression in vivo of the two myogenic regulatory factors, Myf5 and MyoD during this process. Cardiotoxin was used to induce regeneration in the gastrocnemius and soleus muscles of heterozygous Myf5-nlacZ mice, and the muscles were assayed for the presence of (beta)-galactosidase (Myf5) and MyoD. Adult satellite cells identified by M-cadherin labelling, when activated, initially express either MyoD or Myf5 or both myogenic factors. Subsequently all proliferating myoblasts express MyoD and part of the population is (beta)-galactosidase (Myf5) positive. Furthermore, we demonstrate that activated satellite cells, which express either Myf5 or MyoD, do not accumulate selectively on fast or slow muscle fibres.

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.”

Heat stress increases myonuclear number and fiber size via satellite cell activation in rat regenerating soleus fibers

2009 ◽  
Vol 107 (5) ◽  
pp. 1612-1621 ◽  
Author(s):  
Yasuharu Oishi ◽  
Mari Hayashida ◽  
Shinsuke Tsukiashi ◽  
Kohachi Taniguchi ◽  
Katsuya Kami ◽  
...  
Keyword(s):  
Heat Stress ◽  
Satellite Cells ◽  
Cell Activation ◽  
The Body ◽  
Muscle Weight ◽  
Cross Sectional ◽  
Time Points ◽  
Protein Levels ◽  
Male Wistar Rats ◽  
Satellite Cell Activation

To investigate the effects of heat stress (hyperthermia) on muscle degeneration-regeneration, the soleus muscles of adult male Wistar rats were injected bilaterally with a single injection of bupivacaine. The rats were assigned to a sedentary control (Con), heat stress (Heat), bupivacaine-injected (BPVC), or bupivacaine-injected plus heat stress (BPVC+Heat) group. Heat stress was induced in the Heat and BPVC+Heat groups by immersion of the lower half of the body into water maintained at 42 ± 1°C for 30 min 48 h after the injection of bupivacaine and every other day during the following 1 or 2 wk. The soleus muscles in all groups were excised 24 h after the final bout of heat stress. Mean muscle weight, fiber cross-sectional area, myonuclear number, and heat shock protein 72 (Hsp72) and calcineurin protein levels were lower in the BPVC than in the Con or Heat groups at both time points. In contrast, several of these parameters in the BPVC+Heat group were not different or higher than in the Con or Heat groups at the 1- and/or 2-wk time points. The number of total and activated satellite cells, estimated by analyses of Pax7-negative, M-cadherin-negative, and MyoD-positive nuclei, was greater in BPVC+Heat than in all other groups. Combined, the results indicate that heat stress-related activation of satellite cells and upregulation of Hsp72 and calcineurin expression played important roles in the regeneration of the soleus fibers after bupivacaine injection.

scholarly journals Culture conditions influence satellite cell activation and survival of single myofibers

2018 ◽  
Vol 28 (2) ◽  
Author(s):  
Alessandra Renzini ◽  
Anna Benedetti ◽  
Marina Bouché ◽  
Leopoldo Silvestroni ◽  
Sergio Adamo ◽  
...  
Keyword(s):  
Satellite Cell ◽  
Satellite Cells ◽  
Cell Activation ◽  
Culture Conditions ◽  
Experimental Conditions ◽  
Direct Observations ◽  
Satellite Cell Activation ◽  
Indispensable Tool

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.

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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