In Vitro Model for Stretch-Induced Hypertrophy of Skeletal Muscle

Vandenburgh, Herman H.; Kaufman, Seymour

doi:10.1126/science.569901

Cited by 242 publications

(108 citation statements)

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“…Earlier reports have shown that mechanical tension alone can regulate cell growth and metabolism and the intracellular signaling proteins may link changes in the tension to this cellular adaptation (46). Recently it has been shown that mechanical stress stimulates the signaling pathways of ERKs, JNKs, and p38 MAP kinases in a variety of cell lines including skeletal muscle cells (8,9,22,23,29).…”

Section: Figmentioning

confidence: 99%

Distinct Signaling Pathways Are Activated in Response to Mechanical Stress Applied Axially and Transversely to Skeletal Muscle Fibers

Kumar

Chaudhry

Reid

et al. 2002

Journal of Biological Chemistry

112

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In the diaphragm muscle we tested the hypothesis that MAP kinase signaling pathways are activated by mechanical stress and such signaling pathways are dependent on the direction in which mechanical stress is applied. Although equal magnitudes of mechanical stress were applied axially and transversely a greater level of activation of ERK1/2, p38, Raf-1, p90 RSK, Elk-1, and the DNA binding activity of AP-1 transcription factor was produced when the muscle was stretched transversely than when stretched axially. A significant up-regulation in protein tyrosine phosphorylation was observed in axially or transversely loaded diaphragm muscles and the activation of ERK1/2 was completely inhibited by genistein (protein-tyrosine kinase inhibitor). Pretreatment of muscles with wortmannin (phosphoinositide 3-kinase inhibitor), TMB-8 (antagonist of intracellular calcium release), GF109203X (PKC inhibitor), or PD98059 (MEK1/2 inhibitor) blocked the activation of ERK1/2 kinases in response to axial but not to transverse loading. On the other hand, pretreatment of muscles with protein kinase A inhibitors H-7 and KT5720 completely suppressed the activation of ERK1/2 in response to transverse loading only. Taken together with the alterations of MAP kinases and the findings of elevations of downstream transcription targets, our data are consistent with two distinct MAP kinase signal transduction pathways in response to mechanical stress.

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Section: Figmentioning

confidence: 99%

Distinct Signaling Pathways Are Activated in Response to Mechanical Stress Applied Axially and Transversely to Skeletal Muscle Fibers

Kumar

Chaudhry

Reid

et al. 2002

Journal of Biological Chemistry

112

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“…In 1975, Goldberg et al (39) proposed that increased tension development, either passive or active, was the critical event in initiating compensatory growth in mammals. Consistent with the role that mechanical tension plays in regulating skeletal muscle mass in vivo, stretch models have been used to demonstrate that mechanical tension also regulates protein synthesis in vitro (97)(98)(99). Using a cell culture model, Vandenburgh and Kaufman (97,98) demonstrated that intermittent stretch produces a large increase in protein synthesis and a smaller decrease in protein degradation in avian myotubes.…”

mentioning

confidence: 99%

“…Consistent with the role that mechanical tension plays in regulating skeletal muscle mass in vivo, stretch models have been used to demonstrate that mechanical tension also regulates protein synthesis in vitro (97)(98)(99). Using a cell culture model, Vandenburgh and Kaufman (97,98) demonstrated that intermittent stretch produces a large increase in protein synthesis and a smaller decrease in protein degradation in avian myotubes. These data suggest that in cell culture, like models in vivo, the hypertrophic response to increased mechanical tension is due, in part, to an increased rate of protein synthesis.…”

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confidence: 99%

Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals

Miyazaki

Esser²

2009

Journal of Applied Physiology

164

142

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Miyazaki M, Esser KA. Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals. J Appl Physiol 106: 1367-1373, 2009; doi:10.1152/japplphysiol.91355.2008.-Growth and maintenance of skeletal muscle mass is critical for long-term health and quality of life. Skeletal muscle is a highly adaptable tissue with well-known sensitivities to environmental cues such as growth factors, cytokines, nutrients, and mechanical loading. All of these factors act at the level of the cell and signal through pathways that lead to changes in phenotype through multiple mechanisms. In this review, we discuss the animal and cell culture models used and the signaling mechanisms identified in understanding regulation of protein synthesis in response to mechanical loading/resistance exercise. Particular emphasis has been placed on 1) alterations in mechanical loading and regulation of protein synthesis in both in vivo animal studies and in vitro cell culture studies and 2) upstream mediators regulating mammalian target of rapamycin signaling and protein synthesis during skeletal muscle hypertrophy. mechanical stretch; REDD2; overload; IGF-1; amino acids IT IS WIDELY ACCEPTED that repeated bouts of resistance exercise/ high-force contractions produce compensatory growth of skeletal muscle (35,42,47,95). The increase in skeletal muscle mass results from rates of protein synthesis increased more than changes in protein degradation with the net result being an accumulation of protein and increased fiber area (66,96). While the effect of resistance exercise/contraction on muscle mass has long been recognized, the mechanisms underlying the link between high resistance contractions and muscle growth are, to date, not fully understood.One of the important variables contributing to the growth response in skeletal muscle is the application of mechanical loading. For this review we use mechanical loading very generally as the application of force on the muscle or muscle cell. This force on the muscle can occur via active cross-bridge interactions (such as during concentric, isometric, or eccentric contractions) in a gravity-based environment or via external application of force such as passive stretching. The most established animal model for studying skeletal muscle hypertrophy in response to mechanical loading was described by Dr. A. L. Goldberg (38) and was referred to as work-induced muscle growth. This model is now commonly known as the synergist ablation/mechanical overload model and is a surgical model that involves cutting of the tendon and removal of the gastrocnemius muscle, resulting in loading and compensatory growth of the remaining plantar flexors, the plantaris, and soleus muscles. These muscles are involved in maintenance of posture and walking so are loaded by the body weight of the animal. Muscle mass changes are fairly rapid and the growth is robust, ranging from 40 to 200% depending on the muscle and species studied (7,37,38,53,56). Many labs use this model in their research programs to study mole...

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“…Cells in areas of airspace remodeling likely are subjected to significant alterations in physical and mechanical stress that might play an inductive role. Work on striated muscle has established a dependency of differentiation-specific proteins on generation of tension [Vandenburgh and Kaufman, 1979;Crisona and Strohman, 1983;Riley et al, 19901 and mechanical forces also may regulate matrix production. Recent studies by Kapanci et al [1990] underscore the potential importance of mechanical forces in lung remodeling in that post-capillary hypertension appears to induce SMaA expression in cells of the alveolar wall, perhaps in the cellular actin-containing contractile interstitial cell.…”

Section: The Origin Of Lung Myofibroblastsmentioning

confidence: 99%