Satellite cells are increasingly refractory to activation by nitric oxide and stretch in aged mouse-muscle cultures

2010 ◽  
Vol 42 (1) ◽  
pp. 132-136 ◽  
Author(s):  
Jeff R.S. Leiter ◽  
Judy E. Anderson
Keyword(s):  
Nitric Oxide ◽  
Satellite Cells ◽  
Aged Mouse ◽  
Mouse Muscle ◽  
Muscle Cultures

Sex, fiber-type, and age dependent in vitro proliferation of mouse muscle satellite cells

2011 ◽  
Vol 112 (10) ◽  
pp. 2825-2836 ◽  
Author(s):  
Raquel Manzano ◽  
Janne M. Toivonen ◽  
Ana C. Calvo ◽  
Francisco J. Miana-Mena ◽  
Pilar Zaragoza ◽  
...  
Keyword(s):  
Satellite Cells ◽  
Fiber Type ◽  
In Vitro Proliferation ◽  
Mouse Muscle ◽  
Muscle Satellite Cells ◽  
Age Dependent

Neural cell adhesion molecule in aged mouse muscle

Neuroscience ◽  
1992 ◽  
Vol 48 (1) ◽  
pp. 237-248 ◽  
Author(s):  
H. Kobayashi ◽  
N. Robbins ◽  
U. Rutishauser
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Neural Cell ◽  
Aged Mouse ◽  
Mouse Muscle ◽  
Neural Cell Adhesion

Single-fiber isolation and maintenance of satellite cell quiescence

2005 ◽  
Vol 83 (5) ◽  
pp. 674-676 ◽  
Author(s):  
Ashley C Wozniak ◽  
Judy E Anderson
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Muscle Fibers ◽  
Single Fiber ◽  
Skeletal Muscle Regeneration ◽  
Mouse Muscle ◽  
Collagenase Digestion ◽  
Cell Quiescence ◽  
Gentle Agitation

The activity of satellite cells during myogenesis, development, or skeletal muscle regeneration is strongly modelled using cultures of single muscle fibers. However, there are variations in reported features of gene or protein expression as examined with single-fiber cultures. Here, we examined the potential differences in activation of satellite cells on normal mouse muscle fibers produced during a standard isolation protocol, with or without agitation during collagenase digestion. Activation was detected in satellite cells on fibers after 24 and 48 h of culture in basal growth medium using immunodetection of the incorporation of bromodeoxyuridine (BrdU) into DNA and quantification of the number of BrdU-positive cells per fiber. After 24 and 48 h in culture under nonactivating conditions, the number of activated (BrdU+) satellite cells was greater on fibers that had received gentle agitation during collagenase digestion than on those that were subject to digestion without agitation during isolation. The findings are interpreted to mean that at least some of the variation among published reports may derive from the application of various methods of fiber isolation. The information should be useful for maintaining satellite cell quiescence during studies of the regulatory steps that lead to satellite cell activation.Key words: activation, skeletal muscle, proliferation, single-fiber culture, myogenesis.

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.”

scholarly journals Trim33 (Tif1γ) is not required for skeletal muscle development or regeneration but suppresses cholecystokinin expression

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Cassie A. Parks ◽  
Katherine Pak ◽  
Iago Pinal-Fernandez ◽  
Wilson Huang ◽  
Assia Derfoul ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Knockout Mice ◽  
Muscle Regeneration ◽  
Skeletal Muscles ◽  
Muscle Development ◽  
Conditional Knockout ◽  
C2c12 Cells ◽  
Mouse Muscle ◽  
Muscle Histology

AbstractThe expression of Trim33 (Tif1γ) increases in skeletal muscles during regeneration and decreases upon maturation. Although Trim33 is required for the normal development of other tissues, its role in skeletal muscle is unknown. The current study aimed to define the role of Trim33 in muscle development and regeneration. We generated mice with muscle-specific conditional knockout of Trim33 by combining floxed Trim33 and Cre recombinase under the Pax7 promoter. Muscle regeneration was induced by injuring mouse muscles with cardiotoxin. We studied the consequences of Trim33 knockdown on viability, body weight, skeletal muscle histology, muscle regeneration, and gene expression. We also studied the effect of Trim33 silencing in satellite cells and the C2C12 mouse muscle cell line. Although Trim33 knockdown mice weighed less than control mice, their skeletal muscles were histologically unremarkable and regenerated normally following injury. Unexpectedly, RNAseq analysis revealed dramatically increased expression of cholecystokinin (CCK) in regenerating muscle from Trim33 knockout mice, satellite cells from Trim33 knockout mice, and C2C12 cells treated with Trim33 siRNA. Trim33 knockdown had no demonstrable effect on muscle differentiation or regeneration. However, Trim33 knockdown induced CCK expression in muscle, suggesting that suppression of CCK expression requires Trim33.

scholarly journals Further Characterisation of the Molecular Signature of Quiescent and Activated Mouse Muscle Satellite Cells

PLoS ONE ◽  
2009 ◽  
Vol 4 (4) ◽  
pp. e5205 ◽  
Author(s):  
Viola F. Gnocchi ◽  
Robert B. White ◽  
Yusuke Ono ◽  
Juliet A. Ellis ◽  
Peter S. Zammit
Keyword(s):  
Satellite Cells ◽  
Molecular Signature ◽  
Mouse Muscle ◽  
Muscle Satellite Cells
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