scholarly journals Cultured equine satellite cells as a model system to assess leucine stimulated protein synthesis in horse muscle

2018 ◽  
Vol 96 (1) ◽  
pp. 143-153 ◽  
Author(s):  
Michelle L DeBoer ◽  
Krishona M Martinson ◽  
Mary S Pampusch ◽  
Abigail M Hansen ◽  
Scott M Wells ◽  
...  
2017 ◽  
Vol 52 ◽  
pp. 92-93
Author(s):  
M.L. DeBoer ◽  
K.L. Martinson ◽  
M.S. Wells ◽  
C. Ward ◽  
M.R. Hathaway

2011 ◽  
Vol 1 (2) ◽  
pp. 52-61
Author(s):  
Bernardo Neme Ide ◽  
Fernanda Lorenzi Lazarim ◽  
Denise Vaz de Macedo

A resposta adaptativa ao treinamento físico é determinada pelo tipo, volume e frequência de aplicação dos estímulos, que ativam vias de sinalização distintas, a transcrição de genes específicos e posterior síntese protéica. O treinamento resistido está relacionado à ativação da enzima mTOR, proporcionada pelo hormônio IGF-1 e estimulada pela insulina, quando um carboidrato é consumido após a atividade física. Estas vias de sinalização levam à inibição da transcrição de genes relacionados à atrofia e aumento da síntese de proteínas contráteis e metabólicas, proporcionando um aumento da massa muscular, conhecido como hipertrofia. Atualmente, evidências sugerem que, além das sinalizações dos hormônios, os estímulos mecânicos (mecanotransdução) também podem influenciar a ativação gênica durante o processo hipertrófico. A ativação de células satélites, proporcionada pelo estresse mecânico, fatores de crescimento, radicais livres e citocinas é de suma importância para o crescimento muscular. Devido à relevância deste assunto, o presente trabalho traz uma revisão da literatura a respeito dos processos envolvidos na resposta hipertrófica, em decorrência do treinamento físico. Embora o processo hipertrófico seja bastante estudado, os mecanismos moleculares, tanto em nível gênico quanto protéico, envolvidos no processo adaptativo ainda não são totalmente compreendidos. Neste sentido, o avanço nas técnicas de biologia molecular como genômica, transcriptoma e proteômica abrem caminhos para futuras investigações nesta área.Palavras-chave: treino resistido, adaptações ao treinamento de força, células satélites, IGF-1, síntese protéica.The adaptation process to physical training is determined by the type, volume and frequency of stimulation, activating distinct signaling pathways, specific gene transcription and then protein synthesis. Resistance-training is related to mTOR enzyme activation induced by IGF-1 and stimulated by insulin when carbohydrates are consumed after physical activity. These pathways, may lead to the inhibition of gene transcription related to atrophy and the increment of contractile and metabolic protein synthesis causing an increase on muscle mass known as hypertrophy. Presently, there is evidence to suggest that besides hormone signaling pathways, mechanical stimulation (mechanotransduction) may also influence the gene activation during the hypertrophic process. The satellite cells activation induced by mechanical stress, growth factors, free radicals, and cytokines is crucial for muscle growth. Due to the importance of this topic, the present study, proposes a literature review about the processes related to the hypertrophic responses to physical training. Despite the frequent studies on the hypertrophic process, the molecular mechanisms (both at gene and protein levels) involved in the adaptation process is yet to be fully understood. Thus, advances in molecular biology techniques such as genomic, transcriptoma and proteomic open ways for future investigations in this area.Key words: Resistance-training, strength training adaptations, satellite cells, IGF-1, protein synthesis.


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.


1990 ◽  
Vol 18 (4a) ◽  
pp. 511-512 ◽  
Author(s):  
Robert A. Haworth ◽  
Atilla B. Goknur ◽  
Melissa G. Cook ◽  
Robert S. Decker

The usefulness of isolated adult cardiac myocytes, both in suspension and in culture, as a model system for measuring cardiotoxicity is evaluated. It has been suggested that isolated adult myocytes should preferably be cultured for such experimentation, as this restores the cells to a physiological preference for fatty acids as a substrate rather than glucose. We show here that the restoration of Ca2+ to cells immediately after isolation results in an artificially enhanced glucose metabolism, as measured by an elevated rate of deoxyglucose uptake. Early restoration of Ca2+ during cell isolation, on the other hand, results in cells with a normal low level of deoxyglucose uptake. We, thus, conclude that cells can be ready for valid toxicity studies immediately after isolation, without the need for culture. The culture of adult feline ventricular cells is also described. These cells, like rabbit but unlike rat, are particularly promising for toxicity studies because they remain quiescent in culture and do not round up. On exposure to norepinephrine, they beat spontaneously and increase their rate of protein synthesis.


1989 ◽  
Vol 122 (2) ◽  
pp. 565-571 ◽  
Author(s):  
J. A. Roe ◽  
J. M. M. Harper ◽  
P. J. Buttery

ABSTRACT Methods were developed for the isolation and culture of satellite cells from adult sheep muscle. Differentiated cultures of these cells were used to investigate the effects of four hormones and growth factors on protein synthesis and degradation. Insulin was found to have no effect except at supraphysiological concentrations (100 nmol/l and 1 μmol/l) where it is probably cross-reacting with the insulin-like growth factor (IGF) type-I receptor. IGF-I was found to be anabolic at lower concentrations (1–3 nmol/l). Epidermal growth factor (EGF) had a smaller effect on protein synthesis and degradation than insulin or IGF-I. The specific activity of the muscle-specific enzyme creatine phosphokinase (CPK) was increased by treatment with EGF. When both IGF-I and EGF were present in the test media an additive effect on protein synthesis was observed. However, no additive effect of IGF-I and insulin was noted. No effects of bovine GH were seen. Journal of Endocrinology (1989) 122, 565–571


2020 ◽  
Author(s):  
Ryo Fujita ◽  
Graham Lean ◽  
Solène Jamet ◽  
Steven Hébert ◽  
Claudia L. Kleinman ◽  
...  

AbstractTranslational control of gene expression is an important regulator of adult stem cell quiescence, activation and self-renewal. In skeletal muscle, quiescent satellite cells maintain low levels of protein synthesis, mediated in part through the phosphorylation of eIF2α (P-eIF2α). Pharmacological inhibition of the eIF2α phosphatase with the small molecule sal003 maintains P-eIF2α and permits the expansion of satellite cells ex vivo. Paradoxically, P-eIF2α also increases the translation of specific mRNAs, which is mediated by P-eIF2α dependent readthrough of inhibitory upstream open reading frames (uORFs). Here, we ask whether P-eIF2α dependent mRNA translation enables expansion of satellite cells. Using transcriptomic and proteomic analyses, we show a number of genes associated with the assembly of the spindle pole to be upregulated at the level of protein, without corresponding change in mRNA levels, in satellite cells expanded in the presence of sal003. We show that uORFs in the 5’UTR of mRNA for the mitotic spindle stability gene Tacc3 direct P-eIF2α dependent translation. Satellite cells deficient for TACC3 exhibit defects in expansion, self-renewal and regeneration of skeletal muscle.SignificanceTranslational control of gene expression has emerged as an important regulator of adult stem cell populations, which maintain low levels of protein synthesis. In adult muscle stem cells, or satellite cells, a portrait of translational control has emerged whereby multiple repression mechanisms prevent the translation of specific mRNAs. It remains unclear how other mRNAs escape repression and are efficiently translated. We show that within the context of low global rates of protein synthesis, satellite cell expansion occurs through the selective translation of Tacc3 mRNA. Tacc3 deficient satellite cells expand poorly, leading to defects in skeletal muscle regeneration. Our study provides a more complete picture of translational control of gene expression in adult stem cell populations.


2011 ◽  
Vol 11 (2) ◽  
pp. 139-146 ◽  
Author(s):  
Dong Wang ◽  
Nam V. Vo ◽  
Gwendolyn A. Sowa ◽  
Robert A. Hartman ◽  
Kevin Ngo ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document