Dual effect of HGF on satellite/myogenic cell quiescence. Focus on “High concentrations of HGF inhibit skeletal muscle satellite cell proliferation in vitro by inducing expression of myostatin: a possible mechanism for reestablishing satellite cell quiescence in vivo”

2010 ◽  
Vol 298 (3) ◽  
pp. C448-C449 ◽  
Author(s):  
Bénédicte Chazaud
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Satellite Cell ◽  
Dual Effect ◽  
Cell Quiescence ◽  
High Concentrations ◽  
Skeletal Muscle Satellite Cell ◽  
Proliferation In Vitro

Oxygen-mediated regulation of skeletal muscle satellite cell proliferation and adipogenesis in culture

2001 ◽  
Vol 189 (2) ◽  
pp. 189-196 ◽  
Author(s):  
Marie Csete ◽  
Jean Walikonis ◽  
Nicole Slawny ◽  
Yuewang Wei ◽  
Sheryl Korsnes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Muscle Satellite Cell ◽  
Satellite Cell Proliferation ◽  
Skeletal Muscle Satellite Cell

scholarly journals PEDF-derived peptide promotes skeletal muscle regeneration through its mitogenic effect on muscle progenitor cells

2015 ◽  
Vol 309 (3) ◽  
pp. C159-C168 ◽  
Author(s):  
Tsung-Chuan Ho ◽  
Yi-Pin Chiang ◽  
Chih-Kuang Chuang ◽  
Show-Li Chen ◽  
Jui-Wen Hsieh ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Cyclin D1 ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Muscle Fibers ◽  
Skeletal Muscle Regeneration ◽  
Satellite Cell Proliferation

In response injury, intrinsic repair mechanisms are activated in skeletal muscle to replace the damaged muscle fibers with new muscle fibers. The regeneration process starts with the proliferation of satellite cells to give rise to myoblasts, which subsequently differentiate terminally into myofibers. Here, we investigated the promotion effect of pigment epithelial-derived factor (PEDF) on muscle regeneration. We report that PEDF and a synthetic PEDF-derived short peptide (PSP; residues Ser93-Leu112) induce satellite cell proliferation in vitro and promote muscle regeneration in vivo. Extensively, soleus muscle necrosis was induced in rats by bupivacaine, and an injectable alginate gel was used to release the PSP in the injured muscle. PSP delivery was found to stimulate satellite cell proliferation in damaged muscle and enhance the growth of regenerating myofibers, with complete regeneration of normal muscle mass by 2 wk. In cell culture, PEDF/PSP stimulated C2C12 myoblast proliferation, together with a rise in cyclin D1 expression. PEDF induced the phosphorylation of ERK1/2, Akt, and STAT3 in C2C12 myoblasts. Blocking the activity of ERK, Akt, or STAT3 with pharmacological inhibitors attenuated the effects of PEDF/PSP on the induction of C2C12 cell proliferation and cyclin D1 expression. Moreover, 5-bromo-2′-deoxyuridine pulse-labeling demonstrated that PEDF/PSP stimulated primary rat satellite cell proliferation in myofibers in vitro. In summary, we report for the first time that PSP is capable of promoting the regeneration of skeletal muscle. The signaling mechanism involves the ERK, AKT, and STAT3 pathways. These results show the potential utility of this PEDF peptide for muscle regeneration.

scholarly journals The Skeletal Muscle Satellite Cell: The Stem Cell That Came in From the Cold

2006 ◽  
Vol 54 (11) ◽  
pp. 1177-1191 ◽  
Author(s):  
Peter S. Zammit ◽  
Terence A. Partridge ◽  
Zipora Yablonka-Reuveni
Keyword(s):  
Skeletal Muscle ◽  
Stem Cell ◽  
Satellite Cell ◽  
Muscle Satellite Cell ◽  
Skeletal Muscle Satellite Cell

Development of a Nitric Oxide-Releasing Analogue of the Muscle Relaxant Guaifenesin for Skeletal Muscle Satellite Cell Myogenesis

2009 ◽  
Vol 6 (3) ◽  
pp. 895-904 ◽  
Author(s):  
Guqi Wang ◽  
Frank J. Burczynski ◽  
Brian B. Hasinoff ◽  
Kaidong Zhang ◽  
Qilong Lu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Satellite Cell ◽  
Muscle Relaxant ◽  
Muscle Satellite Cell ◽  
Skeletal Muscle Satellite Cell ◽  
Nitric Oxide Releasing

In vivo expression patterns of MyoD, p21, and Rb proteins in myonuclei and satellite cells of denervated rat skeletal muscle

2004 ◽  
Vol 287 (2) ◽  
pp. C484-C493 ◽  
Author(s):  
Minenori Ishido ◽  
Katsuya Kami ◽  
Mitsuhiko Masuhara
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Time Course ◽  
Kinase Inhibitor ◽  
Expression Patterns ◽  
Cell Types ◽  
Cell Nuclei ◽  
Myogenic Regulatory Factor

MyoD, a myogenic regulatory factor, is rapidly expressed in adult skeletal muscles in response to denervation. However, the function(s) of MyoD expressed in denervated muscle has not been adequately elucidated. In vitro, it directly transactivates cyclin-dependent kinase inhibitor p21 (p21) and retinoblastoma protein (Rb), a downstream target of p21. These factors then act to regulate cell cycle withdrawal and antiapoptotic cell death. Using immunohistochemical approaches, we characterized cell types expressing MyoD, p21, and Rb and the relationship among these factors in the myonucleus of denervated muscles. In addition, we quantitatively examined the time course changes and expression patterns among distinct myofiber types of MyoD, p21, and Rb during denervation. Denervation induced MyoD expression in myonuclei and satellite cell nuclei, whereas p21 and Rb were found only in myonuclei. Furthermore, coexpression of MyoD, p21, and Rb was induced in the myonucleus, and quantitative analysis of these factors determined that there was no difference among the three myofiber types. These observations suggest that MyoD may function in myonuclei in response to denervation to protect against denervation-induced apoptosis via perhaps the activation of p21 and Rb, and function of MyoD expressed in satellite cell nuclei may be negatively regulated. The present study provides a molecular basis to further understand the function of MyoD expressed in the myonuclei and satellite cell nuclei of denervated skeletal muscle.

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