The effect of exercise on IGF-I on muscle fibers and satellite cells

10.2741/e372 ◽  
2012 ◽  
Vol E4 (1) ◽  
pp. 230-239 ◽  
Author(s):  
Dafna Benayahu
Keyword(s):  
Satellite Cells ◽  
Muscle Fibers ◽  
Igf I

Roles of IGF-I and the estrogen, androgen and IGF-I receptors in estradiol-17β- and trenbolone acetate-stimulated proliferation of cultured bovine satellite cells

2008 ◽  
Vol 35 (1) ◽  
pp. 88-97 ◽  
Author(s):  
E. Kamanga-Sollo ◽  
M.E. White ◽  
M.R. Hathaway ◽  
K.Y. Chung ◽  
B.J. Johnson ◽  
...  
Keyword(s):  
Satellite Cells ◽  
Trenbolone Acetate ◽  
Igf I ◽  
Estradiol 17Β

Muscle Fibers in Regenerating Crayfish Motor Nerves

1997 ◽  
Vol 78 (6) ◽  
pp. 3498-3501 ◽  
Author(s):  
Joanne Pearce ◽  
Kristin M. Krause ◽  
C. K. Govind
Keyword(s):  
Signaling Pathway ◽  
Satellite Cells ◽  
Blood Cells ◽  
Axon Regeneration ◽  
Muscle Fibers ◽  
Nerve Terminals ◽  
Motor Axons ◽  
The Third ◽  
Motor Nerves ◽  
Regenerating Nerve

Pearce, Joanne, Kristin M. Krause, and C. K. Govind. Muscle fibers in regenerating crayfish motor nerves. J. Neurophysiol. 78: 3498–3501, 1997. Single discrete muscle fibers were found in regenerating motor nerves in adult crayfish. The regenerating nerves were from native or transplanted ganglia in the third abdominal segments and consisted of several motor axons. The proximal end of these motor axons showed numerous sprouts. Muscle fibers in these regenerating nerves appeared newly developed and were innervated by excitatory nerve terminals. A likely source of these novel muscle fibers may be blood cells in the nerve or satellite cells from neighboring muscle. Contacts made by axon sprouts with other axon sprouts, glia, and muscle fiber, in the form of a dense bar with clustered clear vesicles, characterized the regenerating nerve. These contacts may provide a possible signaling pathway for axon regeneration and myogenesis.

Leucine/glutamic acid/lysine protein 1 is localized to subsets of myonuclei in bovine muscle fibers and satellite cells

2009 ◽  
Vol 87 (10) ◽  
pp. 3134-3141 ◽  
Author(s):  
S. E. Ouellette ◽  
J. Li ◽  
W. Sun ◽  
S. Tsuda ◽  
D. K. Walker ◽  
...  
Keyword(s):  
Glutamic Acid ◽  
Satellite Cells ◽  
Muscle Fibers ◽  
Bovine Muscle

scholarly journals Skeletal muscle regeneration is altered in the R6/2 mouse model of Huntington's disease

2022 ◽  
Author(s):  
Sanzana Hoque ◽  
Marie Sjogren ◽  
Valerie Allamand ◽  
Kinga Gawlik ◽  
Naomi Franke ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Muscle Damage ◽  
Satellite Cell ◽  
Mouse Models ◽  
Satellite Cells ◽  
Muscle Fibers ◽  
Cag Repeat ◽  
Skeletal Muscle Regeneration

Huntington's disease (HD) is caused by CAG repeat expansion in the huntingtin (HTT) gene. Skeletal muscle wasting alongside central pathology is a well-recognized phenomenon seen in patients with HD and HD mouse models. HD muscle atrophy progresses with disease and affects prognosis and quality of life. Satellite cells, progenitors of mature skeletal muscle fibers, are essential for proliferation, differentiation, and repair of muscle tissue in response to muscle injury or exercise. In this study, we aim to investigate the effect of mutant HTT on the differentiation and regeneration capacity of HD muscle by employing in vitro mononuclear skeletal muscle cell isolation and in vivo acute muscle damage model in R6/2 mice. We found that, similar to R6/2 adult mice, neonatal R6/2 mice also exhibit a significant reduction in myofiber width and morphological changes in gastrocnemius and soleus muscles compared to WT mice. Cardiotoxin (CTX)-induced acute muscle damage in R6/2 and WT mice showed that the Pax7+ satellite cell pool was dampened in R6/2 mice at 4 weeks post-injection, and R6/2 mice exhibited an altered inflammatory profile in response to acute damage. Our results suggest that, in addition to the mutant HTT degenerative effects in mature muscle fibers, expression of mutant HTT in satellite cells might alter developmental and regenerative processes to contribute to the progressive muscle mass loss in HD. Taken together, the results presented here encourage further studies evaluating the underlying mechanisms of satellite cell dysfunction in HD mouse models.

Contribution of satellite cells to IGF-I induced hypertrophy of skeletal muscle

1999 ◽  
Vol 167 (4) ◽  
pp. 301-305 ◽  
Author(s):  
Barton-Davis ◽  
Shoturma ◽  
Sweeney
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Igf I

Muscle-specific overexpression of IGF-I improves E-C coupling in skeletal muscle fibers from dystrophic mdx mice

2008 ◽  
Vol 294 (1) ◽  
pp. C161-C168 ◽  
Author(s):  
Jonathan D. Schertzer ◽  
Chris van der Poel ◽  
Thea Shavlakadze ◽  
Miranda D. Grounds ◽  
Gordon S. Lynch
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Muscle Fibers ◽  
Transcript Level ◽  
Direct Result ◽  
Mdx Mice ◽  
Contractile Apparatus ◽  
Dystrophic Muscle ◽  
Insulin Growth Factor ◽  
Igf I

Duchenne muscular dystrophy (DMD) is a lethal X-linked disease caused by the absence of functional dystrophin. Abnormal excitation-contraction (E-C) coupling has been reported in dystrophic muscle fibers from mdx mice, and alterations in E-C coupling components may occur as a direct result of dystrophin deficiency. We hypothesized that muscle-specific overexpression of insulin-growth factor-1 (IGF-I) would reduce E-C coupling failure in mdx muscle. Mechanically skinned extensor digitorum longus muscle fibers from mdx mice displayed a faster decline in depolarization-induced force responses (DIFR); however, there were no differences in sarcoplasmic reticulum (SR)-mediated Ca2+ resequestration or in the properties of the contractile apparatus when compared with nondystrophic controls. The rate of DIFR decline was restored to control levels in fibers from transgenic mdx mice that overexpressed IGF-I in skeletal muscle ( mdx/IGF-I mice). Dystrophic muscles have a lower transcript level of a specific dihydropyridine receptor (DHPR) isoform, and IGF-I-mediated changes in E-C coupling were associated with increased transcript levels of specific DHPR isoforms involved in Ca2+ regulation. Importantly, IGF-I overexpression also increased the sensitivity of the contractile apparatus to Ca2+. The results demonstrate that IGF-I can ameliorate fundamental aspects of E-C coupling failure in dystrophic muscle fibers and that these effects are important for the improvements in cellular function induced by this growth factor.

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.

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