scholarly journals Satellite cell proliferation and skeletal muscle hypertrophy

2006 ◽  
Vol 31 (6) ◽  
pp. 782-790 ◽  
Author(s):  
Gregory R. Adams
Keyword(s):  
Cell Proliferation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Muscle Hypertrophy ◽  
Mononuclear Cells ◽  
Close Association ◽  
Critical Role ◽  
Skeletal Muscle Hypertrophy ◽  
Muscle Loading ◽  
Satellite Cell Proliferation

Satellite cells are small, mononuclear cells found in close association with striated skeletal muscles cells (myofibers). These cells appear to function as reserve myoblasts. A critical role for these cells in the process of muscle regeneration following injury has been clearly established. In that role, satellite cells have been shown to proliferate extensively. Some of the progeny of these cells then fuse with each other to form replacement myofibers, whereas others return to quiescence, thereby maintaining this reserve population. In response to injury, activated satellite cells can also fuse with damaged but viable myofibers to promote repair and regeneration. It has also been observed that satellite cells are activated during periods of significantly increased muscle loading and that some of these cells fuse with apparently undamaged myofibers as part of the hypertrophy process. The observation that the inactivation of satellite cell proliferation prevents most of the hypertrophy response to chronic increases in loading has lead to the hypothesis that a limitation to the expansion of myofiber size is imposed by the number of myonuclei present. Recent evidence suggests that a potential limitation to muscle hypertrophy, in the absence of a reserve supply of myonuclei, may be the inability to sustain increases in ribosomes, thereby limiting translational capacity.

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.

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.

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 Delay in post-ovariectomy estrogen replacement negates estrogen-induced augmentation of post-exercise muscle satellite cell proliferation

2015 ◽  
Vol 93 (11) ◽  
pp. 945-951 ◽  
Author(s):  
Gary Mangan ◽  
Sobia Iqbal ◽  
Andrew Hubbard ◽  
Victoria Hamilton ◽  
Eric Bombardier ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Estrogen Replacement ◽  
Sprague Dawley ◽  
Muscle Satellite Cell ◽  
Post Exercise ◽  
Muscle Satellite Cells ◽  
Satellite Cell Proliferation ◽  
Exercise Muscle

This study examined the effects of a delay in post-ovariectomy replacement of 17β-estradiol (estrogen) on the post-exercise proliferation of muscle satellite cells. Nine-week-old, ovariectomized, female Sprague–Dawley rats (n = 64) were distributed among 8 groups based on estrogen status (0.25 mg estrogen pellet or sham), exercise status (90 min run at 17 m·min–1 and a grade of –13.5° or unexercised), and estrogen replacement (“proximal”, estrogen replacement within 2 weeks; or “delayed”, estrogen replacement at 11 weeks following ovariectomy). Significant increases in satellite cells were found in the soleus and white gastrocnemius muscle (immunofluorescent colocalization of nuclei with Pax7) 72 h following eccentric exercise (p < 0.05) in all exercised groups. Proximal E2 replacement resulted in a further augmentation of muscle satellite cells in exercised rats (p < 0.05) relative to the delayed estrogen replacement group. Expression of PI3K was unaltered and phosphorylation of Akt relative to total Akt increased following estrogen supplementation and exercise. Exercise alone did not alter the expression levels of Akt. An 11 week delay in post-ovariectomy estrogen replacement negated the augmenting influence seen with proximal (2 week delay) post-ovariectomy estrogen replacement on post-exercise muscle satellite cell proliferation. This effect appears to be independent of the PI3K–Akt signaling pathway.

IGF-I restores satellite cell proliferative potential in immobilized old skeletal muscle

2000 ◽  
Vol 89 (4) ◽  
pp. 1365-1379 ◽  
Author(s):  
Manu V. Chakravarthy ◽  
Bradley S. Davis ◽  
Frank W. Booth
Keyword(s):  
Cell Proliferation ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Satellite Cells ◽  
Gastrocnemius Muscle ◽  
Recovery Period ◽  
Proliferative Potential ◽  
Remaining Capacity ◽  
Satellite Cell Proliferation ◽  
Proliferation Potential

One of the key factors responsible for the age-associated reduction in muscle mass may be that satellite cell proliferation potential (number of doublings contained within each cell) could become rate limiting to old muscle regrowth. No studies have tested whether repeated cycles of atrophy-regrowth in aged animals deplete the remaining capacity of satellite cells to replicate or what measures can be taken to prevent this from happening. We hypothesized that there would be a pronounced loss of satellite cell proliferative potential in gastrocnemius muscles of aged rats (25- to 30-mo-old FBN rats) subjected to three cycles of atrophy by hindlimb immobilization (plaster casts) with intervening recovery periods. Our results indicated that there was a significant loss in gastrocnemius muscle mass and in the proliferative potential of the resident satellite cells after just one bout of immobilization. Neither the muscle mass nor the satellite cell proliferation potential recovered from their atrophied values after either the first 3-wk or later 9-wk recovery period. Remarkably, application of insulin-like growth factor I onto the atrophied gastrocnemius muscle for an additional 2 wk after this 9-wk recovery period rescued ∼46% of the lost muscle mass and dramatically increased proliferation potential of the satellite cells from this muscle.

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.

Correlation of serum GH and IGF-1 with satellite cell responsiveness in Targhee rams

1996 ◽  
Vol 62 (1) ◽  
pp. 89-96 ◽  
Author(s):  
M. V. Dodson ◽  
K. L. Hossner ◽  
J. L. Vierck ◽  
B. Mathison ◽  
E. Krabbenhoft
Keyword(s):  
Cell Proliferation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Muscle Growth ◽  
Sampling Period ◽  
Slaughter Weight ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Satellite Cell Proliferation ◽  
Serum Gh

AbstractThis study was performed to assess the relationship between serum growth hormone (GH) and insulin-like growth factor 1 (IGF-1) levels, slaughter weight, and myogenic satellite cell growth kinetics of Targhee rams. Serum was collected from 19 rams at 15-min intervals over a period of 4h. Radioimmunoassays of serum samples for GH revealed considerable variation (within individual rams) over the sampling period, with mean values ranging from 0·63 to 4·88 μg/l (mean overall 2·3 (s.e. 0·33) μg/l; no. = 19). There was no significant correlation between GH levels and slaughter weight (r = −0·11; P > 0·05) at 155 (s.e. 1·08) days. Serum IGF-1 levels of (individual) rams were invariant over the sampling period, with individual means ranging from 62 to 233 μg/l (mean overall of 117 (s.e. 45·6) ugll; no. = 19). IGF-1 was not strongly correlated with slaughter weight (r = +0·35; P > 0·05). Satellite cells were isolated from the left m. semimembranosus of all rams at slaughter and grown in culture to evaluate proliferation amount and differentiation extent. The correlations between serum GH levels and satellite cell proliferation and differentiation in vitro were r = −0·53 (P < 0·05) and r = −0·52 (P < 0·05), respectively. Serum IGF-1 showed no significant correlations to proliferation (r = +0·07; P > 0·05) or to differentiation (r = −0·07; P > 0·05) of the satellite cells. These data suggest that serum GH levels in Targhee rams may not reflect muscle growth potential if correlated to body weight of 155 days. Furthermore, as IGF-1 was not correlated significantly with slaughter weight or to variables of satellite cell proliferation and differentiation, another mode of satellite cell regulation (possibly paracrine controllers) is more likely at play to coordinate the satellite cell involvement in muscle growth in Targhee rams at 155 days.

Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin

2009 ◽  
Vol 297 (1) ◽  
pp. E157-E164 ◽  
Author(s):  
Hélène Gilson ◽  
Olivier Schakman ◽  
Stéphanie Kalista ◽  
Pascale Lause ◽  
Kunihiro Tsuchida ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Muscle Hypertrophy ◽  
Muscle Growth ◽  
Negative Regulator ◽  
Proliferative Capacity ◽  
Muscle Weight ◽  
Satellite Cell Proliferation

Follistatin (FS) inhibits several members of the TGF-β superfamily, including myostatin (Mstn), a negative regulator of muscle growth. Mstn inhibition by FS represents a potential therapeutic approach of muscle atrophy. The aim of our study was to investigate the mechanisms of the FS-induced muscle hypertrophy. To test the role of satellite cells in the FS effect, we used irradiation to destroy their proliferative capacity. FS overexpression increased the muscle weight by about 37% in control animals, but the increase reached only 20% in irradiated muscle, supporting the role of cell proliferation in the FS-induced hypertrophy. Surprisingly, the muscle hypertrophy caused by FS reached the same magnitude in Mstn-KO as in WT mice, suggesting that Mstn might not be the only ligand of FS involved in the regulation of muscle mass. To assess the role of activin (Act), another FS ligand, in the FS-induced hypertrophy, we electroporated FSI-I, a FS mutant that does not bind Act with high affinity. Whereas FS electroporation increased muscle weight by 32%, the muscle weight gain induced by FSI-I reached only 14%. Furthermore, in Mstn-KO mice, FSI-I overexpression failed to induce hypertrophy, in contrast to FS. Therefore, these results suggest that Act inhibition may contribute to FS-induced hypertrophy. Finally, the role of Act as a regulator of muscle mass was supported by the observation that ActA overexpression induced muscle weight loss (−15%). In conclusion, our results show that satellite cell proliferation and both Mstn and Act inhibition are involved in the FS-induced muscle hypertrophy.

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.

scholarly journals The Ror1 receptor tyrosine kinase plays a critical role in regulating satellite cell proliferation during regeneration of injured muscle

2017 ◽  
Vol 292 (38) ◽  
pp. 15939-15951 ◽  
Author(s):  
Koki Kamizaki ◽  
Ryosuke Doi ◽  
Makoto Hayashi ◽  
Takeshi Saji ◽  
Motoi Kanagawa ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tyrosine Kinase ◽  
Satellite Cell ◽  
Receptor Tyrosine Kinase ◽  
Critical Role ◽  
Satellite Cell Proliferation
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