scholarly journals Chronic inflammation in skeletal muscle impairs satellite cells function during regeneration: can physical exercise restore the satellite cell niche?

FEBS Journal ◽  
2018 ◽  
Vol 285 (11) ◽  
pp. 1973-1984 ◽  
Author(s):  
Luiz Augusto Perandini ◽  
Patricia Chimin ◽  
Diego da Silva Lutkemeyer ◽  
Niels Olsen Saraiva Câmara
Keyword(s):  
Skeletal Muscle ◽  
Physical Exercise ◽  
Chronic Inflammation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Satellite Cell Niche ◽  
Cell Niche

scholarly journals Syndecan-3 and Notch cooperate in regulating adult myogenesis

2010 ◽  
Vol 190 (3) ◽  
pp. 427-441 ◽  
Author(s):  
Addolorata Pisconti ◽  
D.D.W. Cornelison ◽  
Hugo C. Olguín ◽  
Tiffany L. Antwine ◽  
Bradley B. Olwin
Keyword(s):  
Satellite Cell ◽  
Satellite Cells ◽  
Ectopic Expression ◽  
Postnatal Growth ◽  
Genetic Ablation ◽  
Notch Intracellular Domain ◽  
Satellite Cell Niche ◽  
Cell Niche ◽  
Factor Α ◽  
Molecular Signals

Skeletal muscle postnatal growth and repair depend on satellite cells and are regulated by molecular signals within the satellite cell niche. We investigated the molecular and cellular events that lead to altered myogenesis upon genetic ablation of Syndecan-3, a component of the satellite cell niche. In the absence of Syndecan-3, satellite cells stall in S phase, leading to reduced proliferation, increased cell death, delayed onset of differentiation, and markedly reduced numbers of Pax7+ satellite cells accompanied by myofiber hypertrophy and an increased number of centrally nucleated myofibers. We show that the aberrant cell cycle and impaired self-renewal of explanted Syndecan-3–null satellite cells are rescued by ectopic expression of the constitutively active Notch intracellular domain. Furthermore, we show that Syndecan-3 interacts with Notch and is required for Notch processing by ADAM17/tumor necrosis factor-α–converting enzyme (TACE) and signal transduction. Together, our data support the conclusion that Syndecan-3 and Notch cooperate in regulating homeostasis of the satellite cell population and myofiber size.

scholarly journals Colonization of the Satellite Cell Niche by Skeletal Muscle Progenitor Cells Depends on Notch Signals

2012 ◽  
Vol 23 (3) ◽  
pp. 469-481 ◽  
Author(s):  
Dominique Bröhl ◽  
Elena Vasyutina ◽  
Maciej T. Czajkowski ◽  
Joscha Griger ◽  
Claudia Rassek ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Progenitor Cells ◽  
Satellite Cell ◽  
Satellite Cell Niche ◽  
Muscle Progenitor Cells ◽  
Cell Niche

scholarly journals Thyroid Hormone Receptor Alpha is Essential to Maintain the Satellite Cell Niche During Skeletal Muscle Injury and Sarcopenia of Aging

Thyroid ◽  
2017 ◽  
Vol 27 (10) ◽  
pp. 1316-1322 ◽  
Author(s):  
Anna Milanesi ◽  
Jang-Won Lee ◽  
An Yang ◽  
Yan-Yun Liu ◽  
Sargis Sedrakyan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Satellite Cell ◽  
Hormone Receptor ◽  
Muscle Injury ◽  
Thyroid Hormone Receptor ◽  
Skeletal Muscle Injury ◽  
Receptor Alpha ◽  
Satellite Cell Niche ◽  
Cell Niche

The Satellite Cell Niche in Skeletal Muscle

2017 ◽  
pp. 145-166
Author(s):  
Caroline E. Brun ◽  
Fabien P. Chevalier ◽  
Nicolas A. Dumont ◽  
Michael A. Rudnicki
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Satellite Cell Niche ◽  
Cell Niche

scholarly journals Functional Overload Enhances Satellite Cell Properties in Skeletal Muscle

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Shin Fujimaki ◽  
Masanao Machida ◽  
Tamami Wakabayashi ◽  
Makoto Asashima ◽  
Tohru Takemasa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Physical Exercise ◽  
Resistance Exercise ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Quiescent State ◽  
Proliferative Capacity ◽  
Differentiation Potential ◽  
Activated State

Skeletal muscle represents a plentiful and accessible source of adult stem cells. Skeletal-muscle-derived stem cells, termed satellite cells, play essential roles in postnatal growth, maintenance, repair, and regeneration of skeletal muscle. Although it is well known that the number of satellite cells increases following physical exercise, functional alterations in satellite cells such as proliferative capacity and differentiation efficiency following exercise and their molecular mechanisms remain unclear. Here, we found that functional overload, which is widely used to model resistance exercise, causes skeletal muscle hypertrophy and converts satellite cells from quiescent state to activated state. Our analysis showed that functional overload induces the expression of MyoD in satellite cells and enhances the proliferative capacity and differentiation potential of these cells. The changes in satellite cell properties coincided with the inactivation of Notch signaling and the activation of Wnt signaling and likely involve modulation by transcription factors of the Sox family. These results indicate the effects of resistance exercise on the regulation of satellite cells and provide insight into the molecular mechanism of satellite cell activation following physical exercise.

Implication of the satellite cell in dystrophic muscle fibrosis: a self-perpetuating mechanism of collagen overproduction

2007 ◽  
Vol 293 (2) ◽  
pp. C661-C669 ◽  
Author(s):  
Catherine Alexakis ◽  
Terence Partridge ◽  
George Bou-Gharios
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Collagen Type ◽  
Collagen Type I ◽  
C2c12 Cells ◽  
Type I ◽  
Wild Type ◽  
Dystrophic Muscle ◽  
Type Iii

Because of its mechanical function, skeletal muscle is heavily influenced by the composition of its extracellular matrix (ECM). Fibrosis generated by chronic damage, such as occurs in muscular dystrophies, is thus particularly disastrous in this tissue. Here, we examined the interrelationship between the muscle satellite cell and the production of collagen type I, a major component of fibrotic ECM, by using both C2C12, a satellite cell-derived cell line, and primary muscle satellite cells. In C2C12 cells, we found that expression of collagen type I mRNA decreases substantially during skeletal muscle differentiation. On a single-cell level, collagen type I and myogenin became mutually exclusive after 3 days in differentiation medium, whereas addition of collagen markedly suppressed differentiation of C2C12 cells. Primary cultures of satellite cells associated with isolated single fibers of the young (4 wk old) mdx dystrophic mouse and of C57BL/10ScSn wild-type controls expressed collagen type I and type III mRNA and protein. This pattern persisted in wild-type mice at all ages. But, curiously, in older (18-mo-old) mdx mice, although the myogenic cells continued to express type III collagen, type I expression became restricted to nonmyogenic cells. These cells typically constituted part of a cellular sheet surrounding the old mdx fibers. This combination of features strongly suggests that the progression to fibrosis in dystrophic muscle involves changes in the mechanisms controlling matrix production, which generates positive feedback that results in a reprogramming of myoblasts to a profibrotic function.

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.

scholarly journals Akt1 deficiency diminishes skeletal muscle hypertrophy by reducing satellite cell proliferation

2018 ◽  
Vol 314 (5) ◽  
pp. R741-R751 ◽  
Author(s):  
Nobuki Moriya ◽  
Mitsunori Miyazaki
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Protein Synthesis ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Satellite Cells ◽  
Muscle Hypertrophy ◽  
Mtor Signaling ◽  
Skeletal Muscle Hypertrophy ◽  
Satellite Cell Proliferation

Skeletal muscle mass is determined by the net dynamic balance between protein synthesis and degradation. Although the Akt/mechanistic target of rapamycin (mTOR)-dependent pathway plays an important role in promoting protein synthesis and subsequent skeletal muscle hypertrophy, the precise molecular regulation of mTOR activity by the upstream protein kinase Akt is largely unknown. In addition, the activation of satellite cells has been indicated as a key regulator of muscle mass. However, the requirement of satellite cells for load-induced skeletal muscle hypertrophy is still under intense debate. In this study, female germline Akt1 knockout (KO) mice were used to examine whether Akt1 deficiency attenuates load-induced skeletal muscle hypertrophy through suppressing mTOR-dependent signaling and satellite cell proliferation. Akt1 KO mice showed a blunted hypertrophic response of skeletal muscle, with a diminished rate of satellite cell proliferation following mechanical overload. In contrast, Akt1 deficiency did not affect the load-induced activation of mTOR signaling and the subsequent enhanced rate of protein synthesis in skeletal muscle. These observations suggest that the load-induced activation of mTOR signaling occurs independently of Akt1 regulation and that Akt1 plays a critical role in regulating satellite cell proliferation during load-induced muscle hypertrophy.

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