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

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.

1996 ◽  
Vol 62 (1) ◽  
pp. 89-96 ◽  
Author(s):  
M. V. Dodson ◽  
K. L. Hossner ◽  
J. L. Vierck ◽  
B. Mathison ◽  
E. Krabbenhoft

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.


2018 ◽  
Vol 314 (5) ◽  
pp. R741-R751 ◽  
Author(s):  
Nobuki Moriya ◽  
Mitsunori Miyazaki

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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