scholarly journals Resistance Exercise-Induced Hormonal Response Promotes Satellite Cell Proliferation in Untrained Men

2019 ◽  
Vol 51 (Supplement) ◽  
pp. 78
Author(s):  
Hui-Ying Luk ◽  
Danielle E. Levitt ◽  
James Boyett ◽  
Sharon Rojas ◽  
Shawn M. Flader ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Resistance Exercise ◽  
Satellite Cell ◽  
Hormonal Response ◽  
Satellite Cell Proliferation ◽  
Exercise Induced

LIF is a contraction-induced myokine stimulating human myocyte proliferation

2011 ◽  
Vol 111 (1) ◽  
pp. 251-259 ◽  
Author(s):  
Christa Broholm ◽  
Matthew J. Laye ◽  
Claus Brandt ◽  
Radhika Vadalasetty ◽  
Henriette Pilegaard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Resistance Exercise ◽  
Satellite Cell ◽  
Quadriceps Muscle ◽  
Human Myotubes ◽  
Myoblast Proliferation ◽  
Satellite Cell Proliferation ◽  
Exercise Induced ◽  
Sirna Knockdown

The cytokine leukemia inhibitory factor (LIF) is expressed by skeletal muscle and induces proliferation of myoblasts. We hypothesized that LIF is a contraction-induced myokine functioning in an autocrine fashion to activate gene regulation of human muscle satellite cell proliferation. Skeletal muscle LIF expression, regulation, and action were examined in two models: 1) young men performing a bout of heavy resistance exercise of the quadriceps muscle and 2) cultured primary human satellite cells. Resistance exercise induced a ninefold increase in LIF mRNA content in skeletal muscle, but LIF was not detectable in plasma of the subjects. However, electrically stimulated cultured human myotubes produced and secreted LIF, suggesting that LIF is a myokine with local effects. The well established exercise-induced signaling molecules PI3K, Akt, and mTor contributed to the regulation of LIF in cultured human myotubes as chemical inhibition of PI3K and mTor and siRNA knockdown of Akt1 were independently sufficient to downregulate LIF. Human myoblast proliferation was increased by recombinant exogenous LIF and decreased by siRNA knockdown of the endogenous LIF receptor. Finally, the transcription factors JunB and c-Myc, which promote myoblast proliferation, were induced by LIF in cultured human myotubes. Indeed, both JunB and c-Myc were also increased in skeletal muscle following resistance exercise. Our data suggest that LIF is a contraction-induced myokine, potentially acting in an autocrine or paracrine fashion to promote satellite cell proliferation.

Exercise-enhanced satellite cell proliferation and new myonuclear accretion in rat skeletal muscle

2001 ◽  
Vol 90 (4) ◽  
pp. 1407-1414 ◽  
Author(s):  
Heather K. Smith ◽  
Linda Maxwell ◽  
Carol D. Rodgers ◽  
Nancy H. McKee ◽  
Michael J. Plyley
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Normal Activity ◽  
Adult Skeletal Muscle ◽  
Vastus Intermedius ◽  
Muscle Loading ◽  
Satellite Cell Proliferation ◽  
Exercise Induced

The effects of increased functional loading on early cellular regenerative events after exercise-induced injury in adult skeletal muscle were examined with the use of in vivo labeling of replicating myofiber nuclei and immunocyto- and histochemical techniques. Satellite cell proliferation in the soleus (Sol) of nonexercised rats (0.4 ± 0.2% of fibers) was unchanged after an initial bout of declined treadmill exercise but was elevated after two (1.0 ± 0.2%, P ≤ 0.01), but not four or seven, daily bouts of the same task. Myonuclei produced over the 7-day period comprised 0.9–1.9% of myonuclei in isolated fibers of Sol, tibialis anterior, and vastus intermedius of nonexercised rats. The accretion of new myonuclei was enhanced ( P ≤ 0.05) in Sol and vastus intermedius by the initial exercise followed by normal activity (to 3.1–3.4% of myonuclei) and more so by continued daily exercise (4.2–5.3%). Observed coincident with a lower incidence of histological fiber injury and unchanged fiber diameter and myonuclei per millimeter, the greater new myonuclear accretion induced by continued muscle loading may contribute to an enhanced fiber repair and regeneration after exercise-induced injury.

scholarly journals Glycine Enhances Satellite Cell Proliferation, Cell Transplantation, and Oligonucleotide Efficacy in Dystrophic Muscle

2020 ◽  
Vol 28 (5) ◽  
pp. 1339-1358 ◽  
Author(s):  
Caorui Lin ◽  
Gang Han ◽  
Hanhan Ning ◽  
Jun Song ◽  
Ning Ran ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Satellite Cell ◽  
Cell Transplantation ◽  
Dystrophic Muscle ◽  
Satellite Cell Proliferation

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 Correction to: Micronized sacchachitin promotes satellite cell proliferation through TAK1-JNK-AP-1 signaling pathway predominantly by TLR2 activation

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Meng–Huang Wu ◽  
Chuang–Yu Lin ◽  
Chun–Yin Hou ◽  
Ming–Thau Sheu ◽  
Hsi Chang
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Satellite Cell ◽  
Tlr2 Activation ◽  
Satellite Cell Proliferation

An amendment to this paper has been published and can be accessed via the original article.

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.

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