scholarly journals Thermal stress affects proliferation and differentiation of turkey satellite cells through the mTOR/S6K pathway in a growth-dependent manner

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0262576
Author(s):  
Jiahui Xu ◽  
Gale M. Strasburg ◽  
Kent M. Reed ◽  
Sandra G. Velleman
Keyword(s):  
Thermal Stress ◽  
Satellite Cells ◽  
Muscle Growth ◽  
Control Line ◽  
Dependent Manner ◽  
S6 Kinase ◽  
Downstream Effector ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Irreversible Effects

Satellite cells (SCs) are stem cells responsible for post-hatch muscle growth through hypertrophy and in birds are sensitive to thermal stress during the first week after hatch. The mechanistic target of rapamycin (mTOR) signaling pathway, which is highly responsive to thermal stress in differentiating turkey pectoralis major (p. major) muscle SCs, regulates protein synthesis and the activities of SCs through a downstream effector, S6 kinase (S6K). The objectives of this study were: 1) to determine the effect of heat (43°C) and cold (33°C) stress on activity of the mTOR/S6K pathway in SCs isolated from the p. major muscle of one-week-old faster-growing modern commercial (NC) turkeys compared to those from slower-growing Randombred Control Line 2 (RBC2) turkeys, and 2) to assess the effect of mTOR knockdown on the proliferation, differentiation, and expression of myogenic regulatory factors of the SCs. Heat stress increased phosphorylation of both mTOR and S6K in both turkey lines, with greater increases observed in the RBC2 line. With cold stress, greater reductions in mTOR and S6K phosphorylation were observed in the NC line. Early knockdown of mTOR decreased proliferation, differentiation, and expression of myoblast determination protein 1 and myogenin in both lines independent of temperature, with the RBC2 line showing greater reductions in proliferation and differentiation than the NC line at 38° and 43°C. Proliferating SCs are more dependent on mTOR/S6K-mediated regulation than differentiating SCs. Thus, thermal stress can affect breast muscle hypertrophic potential by changing satellite cell proliferation and differentiation, in part, through the mTOR/S6K pathway in a growth-dependent manner. These changes may result in irreversible effects on the development and growth of the turkey p. major muscle.

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.

scholarly journals miR-194-5p negatively regulates the proliferation and differentiation of rabbit skeletal muscle satellite cells

2020 ◽  
Author(s):  
Yu Shi ◽  
Xudong Mao ◽  
Mingcheng Cai ◽  
Shenqiang Hu ◽  
Xiulan Lai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Mammalian Species ◽  
Muscle Growth ◽  
Luciferase Reporter ◽  
Stem Cell Population ◽  
Muscle Satellite Cells ◽  
Skeletal Muscle Satellite Cells ◽  
Proliferation And Differentiation

Abstract Skeletal muscle satellite cells (SMSCs), also known as a multipotential stem cell population, play a crucial role during muscle growth and regeneration. In recent years, numerous miRNAs have been associated with the proliferation and differentiation of SMSCs in a number of mammalian species; however, the regulatory mechanisms of miR-194-5p in rabbit SMSCs still remain scarce. In this study, miR-194-5p was first observed to be highly expressed in the rabbit leg muscle. Furthermore, both the mimics and inhibitor of miR-194-5p were used to explore its role in the proliferation and differentiation of rabbit SMSCs cultured in vitro. Results from both EdU and CCK8 assays showed that miR-194-5p inhibited the proliferation of SMSCs. Meanwhile, Mef2c was identified as a target gene of miR-194-5p based on the dual-luciferase reporter assay results. In addition, upregulation of miR-194-5p decreased the expression levels of Mef2c and MyoG during rabbit SMSCs differentiation on Days 3 and 7 of in vitro culture. Taken together, these data demonstrated that miR-194-5p negatively regulates the proliferation and differentiation of rabbit SMSCs by targeting Mef2c.

scholarly journals 343 Wnt/β-catenin pathway is required for porcine satellite cell proliferation and differentiation to promote skeletal muscle growth

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 97-97
Author(s):  
Zong-ming Zhang ◽  
Chun-qi Gao ◽  
Hui-chao Yan ◽  
Xiu-qi Wang
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Muscle Growth ◽  
Control Group ◽  
Skeletal Muscle Growth ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Deficiency Group

Abstract Wnt/β-catenin plays a crucial role in skeletal muscle growth, but its specific mechanism still unclear. In this study, due to the distinct role of lysine in pig industry, we provided it as an entry point to investigate the role of Wnt/β-catenin in governing skeletal muscle growth. Firstly, total 18 weaned piglets were divided into three groups: control group, lysine deficiency group and lysine re-supplementation group (lysine levels added from 0.83% to 1.31% at 14 d). After 28 d experiment, all pigs were slaughtered to measure the change of Wnt/β-catenin in skeletal muscle. Secondly, satellite cell (SC) was isolated and cultured with Wnt activator, such as Wnt3a and WRN (Wnt3a, R-spondin1, Noggin) after lysine deficiency for 48 h to investigate cell proliferation and differentiation ability and the level of Wnt/β-catenin in different conditions. The results showed that compared with the control group, lysine deficiency significantly reduced longissimus dorsi muscle weight and Pax7 positive SC, and inhibited Wnt/β-catenin (P &lt; 0.05). Fortunately, these restrictions were rescued to the control levels by lysine re-supplementation (P &gt; 0.05). Meanwhile, compared with the lysine deficiency group, the MTT and western blotting assay showed cell proliferation ability was significantly increased with re-activated Wnt/β-catenin by re-supplemented lysine, Wnt3a or WRN (P &lt; 0.05), respectively. Moreover, under the condition of cell differentiation, compared with the control group, cell fusion index was significantly decreased in the lysine deficiency group (P &lt; 0.05), whereas it was significantly increased with lysine re-supplementation group, Wnt3a or WRN respective supplementation group in comparison with the lysine deficiency group (P &lt; 0.05). In addition, compared with the lysine deficiency group, the protein levels of myogenic regulatory factors and Wnt/β-catenin pathway were also re-activated by re-supplemented lysine, Wnt3a or WRN (P &lt; 0.05). Collectively, we found Wnt/β-catenin activation is required for porcine SC proliferation and differentiation to promote skeletal muscle growth.

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 Consequences of early postnatal lipopolysaccharide exposure on developing lungs in mice

2019 ◽  
Vol 316 (1) ◽  
pp. L229-L244 ◽  
Author(s):  
Amrit Kumar Shrestha ◽  
Matthew L. Bettini ◽  
Renuka T. Menon ◽  
Vashisht Y. N. Gopal ◽  
Shixia Huang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Development ◽  
Dependent Manner ◽  
T Regulatory Cell ◽  
Lung Macrophage ◽  
Flow Cytometric ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Apoptosis ◽  
Proliferation And Differentiation ◽  
The Impact

Bronchopulmonary dysplasia (BPD) is a chronic lung disease of infants that is characterized by interrupted lung development. Postnatal sepsis causes BPD, yet the contributory mechanisms are unclear. To address this gap, studies have used lipopolysaccharide (LPS) during the alveolar phase of lung development. However, the lungs of infants who develop BPD are still in the saccular phase of development, and the effects of LPS during this phase are poorly characterized. We hypothesized that chronic LPS exposure during the saccular phase disrupts lung development by mechanisms that promote inflammation and prevent optimal lung development and repair. Wild-type C57BL6J mice were intraperitoneally administered 3, 6, or 10 mg/kg of LPS or a vehicle once daily on postnatal days (PNDs) 3–5. The lungs were collected for proteomic and genomic analyses and flow cytometric detection on PND6. The impact of LPS on lung development, cell proliferation, and apoptosis was determined on PND7. Finally, we determined differences in the LPS effects between the saccular and alveolar lungs. LPS decreased the survival and growth rate and lung development in a dose-dependent manner. These effects were associated with a decreased expression of proteins regulating cell proliferation and differentiation and increased expression of those mediating inflammation. While the lung macrophage population of LPS-treated mice increased, the T-regulatory cell population decreased. Furthermore, LPS-induced inflammatory and apoptotic response and interruption of cell proliferation and alveolarization was greater in alveolar than in saccular lungs. Collectively, the data support our hypothesis and reveal several potential therapeutic targets for sepsis-mediated BPD in infants.

scholarly journals MicroRNA-19b-3p promotes cell proliferation and osteogenic differentiation of BMSCs by interacting with lncRNA H19

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Gan Xiaoling ◽  
Liu Shuaibin ◽  
Liang Kailu
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Postmenopausal Osteoporosis ◽  
Critical Role ◽  
Dependent Manner ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
17Β Estradiol ◽  
Dose Dependent

Abstract Background To investigated the role of miR-19b-3p in regulating bone marrow mesenchymal stem cell (BMSC) proliferation and osteoblast differentiation. Methods The expression of miR-19b-3p and lncRNA H19 were measured in postmenopausal osteoporosis patients and BMP-22 induced BMSCs using qRT-PCR. MiR-19b-3p mimic or inhibitor was transfected into BMP-2 induced BMSCs. Cell proliferation was measured by BrdU method. Protein expression of RUNX2 and COL1A1 were measured by western blot. PcDNA3.1-lncRNA H19 with or without miR-19b-3p mimic was transfected into BMP-2 induced BMSCs. Results The expression of miR-19b-3p was significantly up-regulated in postmenopausal osteoporosis patients and BMP-2 induced BMSCs. MiR-19b-3p overexpression dramatically elevated, while miR-19b-3p inhibition decreased cell proliferation of BMSCs. Additionally, protein expression levels of RUNX2 and COL1A1, as well as ALP activity were significantly promoted by miR-19b-3p mimic transfection and inhibited by miR-19b-3p inhibitor transfection. LncRNA H19 was obviously down-regulated in postmenopausal osteoporosis patients. H19 overexpression significantly decreased cell proliferation and differentiation by down-regulating miR-19b-3p. Moreover, the expression of miR-19b-3p was inhibited, while H19 elvated in 17β-estradiol (E2) treated BMSCs in a dose-dependent manner. Conclusion These data were the first to reveal the critical role of H19/miR-19b-3p in postmenopausal osteoporosis, and provided a new therapeutic target for OP.

scholarly journals IGF-1 colocalizes with muscle satellite cells following acute exercise in humans

2014 ◽  
Vol 39 (4) ◽  
pp. 514-518 ◽  
Author(s):  
Amanda Grubb ◽  
Sophie Joanisse ◽  
Daniel R. Moore ◽  
Leeann M. Bellamy ◽  
Cameron J. Mitchell ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Growth Factor ◽  
Satellite Cells ◽  
Acute Exercise ◽  
Stem Cell Proliferation ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Exercise In Humans

Insulin-like growth factor-1 (IGF-1) regulates stem cell proliferation and differentiation in vitro. The aim of this study was to quantify the change in satellite cell (SC) specific IGF-1 colocalization following exercise. We observed a significant increase (p < 0.05) in the percentage of SC with IGF-1 colocalization from baseline to 72 h after a bout of resistance exercise. This strongly supports a role for IGF-1 in human SC function following exercise.

scholarly journals Growth Inhibition by Bupivacaine Is Associated with Inactivation of Ribosomal Protein S6 Kinase 1

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Mushtaq Ahmad Beigh ◽  
Mehvish Showkat ◽  
Basharat Bashir ◽  
Asma Bashir ◽  
Mahboob ul Hussain ◽  
...  
Keyword(s):  
Cell Growth ◽  
Ectopic Expression ◽  
Dependent Manner ◽  
S6 Kinase ◽  
Regulatory Pathways ◽  
Downstream Effector ◽  
Mtorc1 Signaling ◽  
The Status ◽  
Long Acting ◽  
Cell Growth And Proliferation

Bupivacaine is an amide type long acting local anesthetic used for epidural anesthesia and nerve blockade in patients. Use of bupivacaine is associated with severe cytotoxicity and apoptosis along with inhibition of cell growth and proliferation. Although inhibition of Erk, Akt, and AMPK seemingly appears to mediate some of the bupivacaine effects, potential downstream targets that mediate its effect remain unknown. S6 kinase 1 is a common downstream effector of several growth regulatory pathways involved in cell growth and proliferation known to be affected by bupivacaine. We have accordingly attempted to relate the growth inhibitory effects of bupivacaine with the status of S6K1 activity and we present evidence that decrease in cell growth and proliferation by bupivacaine is mediated through inactivation of S6 kinase 1 in a concentration and time dependent manner. We also show that ectopic expression of constitutively active S6 kinase 1 imparts substantial protection from bupivacaine induced cytotoxicity. Inactivation of S6K1 though associated with loss of putative mTOR mediated phosphorylation did not correspond with loss of similar phosphorylations in 4EBP1 indicating that S6K1 inhibition was not mediated through inactivation of mTORC1 signaling pathway or its down regulation.

scholarly journals Interactions between p-Akt and Smad3 in injured muscles initiate myogenesis or fibrogenesis

2013 ◽  
Vol 305 (3) ◽  
pp. E367-E375 ◽  
Author(s):  
Yanjun Dong ◽  
Ronak Lakhia ◽  
Sandhya S. Thomas ◽  
Yanlan Dong ◽  
Xiaonan H. Wang ◽  
...  
Keyword(s):  
Satellite Cells ◽  
Nuclear Translocation ◽  
Wild Type Mouse ◽  
Muscle Fibrosis ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Igf I ◽  
Smad3 Phosphorylation ◽  
Tgf Β1 ◽  
Igf Signaling

In catabolic conditions such as aging and diabetes, IGF signaling is impaired and fibrosis develops in skeletal muscles. To examine whether impaired IGF signaling initiates muscle fibrosis, we generated IGF-IR+/− heterozygous mice by crossing loxP-floxed IGF-IR (exon 3) mice with MyoD-cre mice. IGF-IR+/− mice were studied because we were unable to obtain homozygous IGF-IR-KO mice. In IGF-IR+/− mice, both growth and expression of myogenic genes (MyoD and myogenin; markers of satellite cell proliferation and differentiation, respectively) were depressed. Likewise, in injured muscles of IGF-IR+/− mice, there was impaired regeneration, depressed expression of MyoD and myogenin, and increased expression of TGF-β1, α-SMA, collagen I, and fibrosis. To uncover mechanisms stimulating fibrosis, we isolated satellite cells from muscles of IGF-IR+/− mice and found reduced proliferation and differentiation plus increased TGF-β1 production. In C2C12 myoblasts (a model of satellite cells), IGF-I treatment inhibited TGF-β1-stimulated Smad3 phosphorylation, its nuclear translocation, and expression of fibronectin. Using immunoprecipitation assay, we found an interaction between p-Akt or Akt with Smad3 in wild-type mouse muscles and in C2C12 myoblasts; importantly, IGF-I increased p-Akt and Smad3 interaction, whereas TGF-β1 decreased it. Therefore, in muscles of IGF-IR+/− mice, the reduction in IGF-IR reduces p-Akt, allowing for dissociation and nuclear translocation of Smad3 to enhance the TGF-β1 signaling pathway, leading to fibrosis. Thus, strategies to improve IGF signaling could prevent fibrosis in catabolic conditions with impaired IGF signaling.

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