The Molecular Responses of Skeletal Muscle Satellite Cells to Continuous Expression of IGF-1: Implications for the Rescue of Induced Muscular Atrophy in Aged Rats

2001 ◽  
Vol 11 (s1) ◽  
pp. S44-S48 ◽  
Author(s):  
Manu V. Chakravarthy ◽  
Frank W. Booth ◽  
Espen E. Spangenburg
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Molecular Mechanisms ◽  
Muscular Atrophy ◽  
Skeletal Muscle Atrophy ◽  
Molecular Evidence ◽  
Igf I ◽  
Satellite Cell Proliferation

Approximately 50% of humans older than 85 years have physical frailty due to weak skeletal muscles. This indicates a need for determining mechanisms to combat this problem. A critical cellular factor for postnatal muscle growth is a population of myogenic precursor cells called satellite cells. Given the complex process of sarcopenia, it has been postulated that, at some point in this process, a limited satellite cell proliferation potential could become rate-limiting to the regrowth of old muscles. It is conceivable that if satellite cell proliferative capacity can be maintained or enhanced with advanced age, sarcopenia could potentially be delayed or prevented. Therefore, the purposes of this paper are to describe whether IGF-I can prevent muscular atrophy induced by repeated cycles of hindlimb immobilization, increase the in vitro proliferation in satellite cells from these muscles and, if so, the molecular mechanisms by which IGF-1 mediates this increased proliferation. Our results provide evidence that IGFI can enhance aged muscle regrowth possibly through increased satellite cell proliferation. The results also suggest that IGF-I enhances satellite cell proliferation by decreasing the cell cycle inhibitor, p27Kip1, through the PI3’-K/Akt pathway. These data provide molecular evidence for IGF-I’s rescue effect upon aging-associated skeletal muscle atrophy.

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.

Satellite cell proliferation and differentiation during postnatal growth of porcine skeletal muscle

2002 ◽  
Vol 282 (4) ◽  
pp. C899-C906 ◽  
Author(s):  
N. T Mesires ◽  
M. E. Doumit
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Nuclear Antigen ◽  
Positive Staining ◽  
Age Related ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Satellite Cell Proliferation

Age-related changes in satellite cell proliferation and differentiation during rapid growth of porcine skeletal muscle were examined. Satellite cells were isolated from hindlimb muscles of pigs at 1, 7, 14, and 21 wk of age (4 animals/age group). Satellite cells were separated from cellular debris by using Percoll gradient centrifugation and were adsorbed to glass coverslips for fluorescent immunostaining. Positive staining for neural cell adhesion molecule (NCAM) distinguished satellite cells from nonmyogenic cells. The proportion of NCAM-positive cells (satellite cells) in isolates decreased from 1 to 7 wk of age. Greater than 77% of NCAM-positive cells were proliferating cell nuclear antigen positive at all ages studied. Myogenin-positive satellite cells decreased from 30% at 1 wk to 14% at 7 wk of age and remained at constant levels thereafter. These data indicate that a high percentage of satellite cells remain proliferative during rapid postnatal muscle growth. The reduced proportion of myogenin-positive cells during growth may reflect a decrease in the proportion of differentiating satellite cells or accelerated incorporation of myogenin-positive cells into myofibers.

scholarly journals microRNA-1 and microRNA-206 regulate skeletal muscle satellite cell proliferation and differentiation by repressing Pax7

2010 ◽  
Vol 190 (5) ◽  
pp. 867-879 ◽  
Author(s):  
Jian-Fu Chen ◽  
Yazhong Tao ◽  
Juan Li ◽  
Zhongliang Deng ◽  
Zhen Yan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Cell Differentiation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Adult Stem Cells ◽  
Myoblast Differentiation ◽  
Proliferative Potential ◽  
Satellite Cell Proliferation

Skeletal muscle satellite cells are adult stem cells responsible for postnatal skeletal muscle growth and regeneration. Paired-box transcription factor Pax7 plays a central role in satellite cell survival, self-renewal, and proliferation. However, how Pax7 is regulated during the transition from proliferating satellite cells to differentiating myogenic progenitor cells is largely unknown. In this study, we find that miR-1 and miR-206 are sharply up-regulated during satellite cell differentiation and down-regulated after muscle injury. We show that miR-1 and miR-206 facilitate satellite cell differentiation by restricting their proliferative potential. We identify Pax7 as one of the direct regulatory targets of miR-1 and miR-206. Inhibition of miR-1 and miR-206 substantially enhances satellite cell proliferation and increases Pax7 protein level in vivo. Conversely, sustained Pax7 expression as a result of the loss of miR-1 and miR-206 repression elements at its 3′ untranslated region significantly inhibits myoblast differentiation. Therefore, our experiments suggest that microRNAs participate in a regulatory circuit that allows rapid gene program transitions from proliferation to differentiation.

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

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 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.

Early-age heat exposure affects skeletal muscle satellite cell proliferation and differentiation in chicks

2001 ◽  
Vol 281 (1) ◽  
pp. R302-R309 ◽  
Author(s):  
Orna Halevy ◽  
Alon Krispin ◽  
Yael Leshem ◽  
John P. McMurtry ◽  
Shlomo Yahav
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Satellite Cell ◽  
Heat Exposure ◽  
Muscle Growth ◽  
Significant Difference ◽  
Igf I ◽  
Satellite Cell Proliferation ◽  
Skeletal Muscle Satellite Cell

Exposure of young chicks to thermal conditioning (TC; i.e., 37°C for 24 h) resulted in significantly improved body and muscle growth at a later age. We hypothesized that TC causes an increase in satellite cell proliferation, necessary for further muscle hypertrophy. An immediate increase was observed in satellite cell DNA synthesis in culture and in vivo in response to TC of 3-day-old chicks to levels that were significantly higher than those of control chicks. This was accompanied by a marked induction of insulin-like growth factor-I (IFG-I), but not hepatocyte growth factor in the breast muscle. No significant difference between treatments in plasma IGF-I levels was observed. A marked elevation in muscle regulatory factors on day 5, followed by a decline in cell proliferation on day 6together with continuous high levels of IGF-I in the TC chick muscle may indicate accelerated cell differentiation. These data suggest a central role for IGF-I in the immediate stimulation of satellite cell myogenic processes in response to heat exposure.

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.

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