scholarly journals Interactions between β-enolase and creatine kinase in the cytosol of skeletal muscle cells

2000 ◽  
Vol 346 (1) ◽  
pp. 127-131 ◽  
Author(s):  
Georges FOUCAULT ◽  
Monique VACHER ◽  
Sophie CRIBIER ◽  
Martine ARRIO-DUPONT
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Diffusion Coefficient ◽  
Weak Interaction ◽  
Satellite Cells ◽  
Fringe Pattern ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Skinned Fibres

We studied interactions in vivo between the cytosolic muscle isoform of creatine kinase (M-CK) and the muscle isoform of 2-phospho-D-glycerate hydrolyase (β-enolase) in muscle sarcoplasm by incubating glycerol-skinned fibres with FITC-labelled β-enolase in the presence or absence of free CK. A small amount of bound β-enolase was observed in the presence of large concentrations of CK. The mobility of enolase was measured in cultured satellite cells by modulated-fringe-pattern photobleaching. FITC-labelled β-enolase was totally mobile in both the presence and the absence of CK but its diffusion coefficient was slightly lower in the presence of CK. This suggests a weak interaction in vivo between enolase and CK.

IL-7 is expressed and secreted by human skeletal muscle cells

2010 ◽  
Vol 298 (4) ◽  
pp. C807-C816 ◽  
Author(s):  
Fred Haugen ◽  
Frode Norheim ◽  
Henrik Lian ◽  
Andreas J. Wensaas ◽  
Svein Dueland ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Myosin Heavy Chain ◽  
Real Time ◽  
Satellite Cells ◽  
Heavy Chain ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Rt Pcr ◽  
Human Myotubes

In addition to generating movement, skeletal muscle may have a function as a secretory organ. The aim of the present study was to identify novel proteins with signaling capabilities secreted from skeletal muscle cells. IL-7 was detected in media conditioned by primary cultures of human myotubes differentiated from satellite cells, and concentrations increased with incubation time. By immunoblotting and real-time RT-PCR IL-7 expression was confirmed at both protein and mRNA levels. Furthermore, with immunofluorescence and specific antisera, multinucleated myotubes were found to coexpress IL-7 and myosin heavy chain. During differentiation of human myotubes from satellite cells, IL-7 expression increased at mRNA and protein levels. In contrast, mRNA expression of the IL-7 receptor was 80% lower in myotubes compared with satellite cells. Incubations with recombinant IL-7 under differentiation conditions caused ∼35% reduction in mRNA for the terminal myogenic markers myosin heavy chain 2 (MYH2) and myogenin (MYOG), suggesting that IL-7 may act on satellite cells to inhibit development of the muscle fiber phenotype. Alternative routes of cell development were investigated, and IL-7 increased migration of satellite cells by 40% after 48 h in a Transwell system, whereas cell proliferation remained unchanged. In vivo, real-time RT-PCR analysis of musculus vastus lateralis ( n = 10) and musculus trapezius ( n = 7) biopsies taken from male individuals undergoing a strength training program demonstrated that after 11 wk mean IL-7 mRNA increased by threefold ( P = 0.01) and fourfold ( P = 0.04), respectively. In conclusion, we have demonstrated that IL-7 is a novel myokine regulated both in vitro and in vivo, and it may play a role in the regulation of muscle cell development.

ALY688 elicits adiponectin-mimetic signaling and improves insulin action in skeletal muscle cells

2021 ◽  
Author(s):  
Hye Kyoung Sung ◽  
Patricia L. Mitchell ◽  
Sean Gross ◽  
Andre Marette ◽  
Gary Sweeney
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Muscle Cells ◽  
Temporal Analysis ◽  
Skeletal Muscle Cells ◽  
Adiponectin Receptor ◽  
Metabolic Effects

Adiponectin is well established to mediate many beneficial metabolic effects, and this has stimulated great interest in development and validation of adiponectin receptor agonists as pharmaceutical tools. This study investigated the effects of ALY688, a peptide-based adiponectin receptor agonist, in rat L6 skeletal muscle cells. ALY688 significantly increased phosphorylation of several adiponectin downstream effectors, including AMPK, ACC and p38MAPK, assessed by immunoblotting and immunofluorescence microscopy. Temporal analysis using cells expressing an Akt biosensor demonstrated that ALY688 enhanced insulin sensitivity. This effect was associated with increased insulin-stimulated Akt and IRS-1 phosphorylation. The functional metabolic significance of these signaling effects was examined by measuring glucose uptake in myoblasts stably overexpressing the glucose transporter GLUT4. ALY688 treatment both increased glucose uptake itself and enhanced insulin-stimulated glucose uptake. In the model of high glucose/high insulin (HGHI)-induced insulin resistant cells, both temporal studies using the Akt biosensor as well as immunoblotting assessing Akt and IRS-1 phosphorylation indicated that ALY688 significantly reduced insulin resistance. Importantly, we observed that ALY688 administration to high-fat high sucrose fed mice also improve glucose handling, validating its efficacy in vivo. In summary, these data indicate that ALY688 activates adiponectin signaling pathways in skeletal muscle, leading to improved insulin sensitivity and beneficial metabolic effects.

scholarly journals Interactions between β-enolase and creatine kinase in the cytosol of skeletal muscle cells

2000 ◽  
Vol 346 (1) ◽  
pp. 127 ◽  
Author(s):  
Georges FOUCAULT ◽  
Monique VACHER ◽  
Sophie CRIBIER ◽  
Martine ARRIO-DUPONT
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

scholarly journals THE FINE STRUCTURE OF EMBRYONIC CHICK SKELETAL MUSCLE CELLS DIFFERENTIATED IN VITRO

1967 ◽  
Vol 35 (2) ◽  
pp. 445-453 ◽  
Author(s):  
Y. Shimada ◽  
D. A. Fischman ◽  
A. A. Moscona
Keyword(s):  
Electron Microscopy ◽  
Skeletal Muscle ◽  
Fine Structure ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Chick Embryos ◽  
Embryonic Chick ◽  
Developing Muscle

Dissociated myoblasts from 12-day chick embryos were cultured in monolayer, and the differentiation of skeletal muscle cells was studied by electron microscopy. The results have revealed a striking ultrastructural similarity between the in vivo and the in vitro developing muscle, particularly with respect to the myofibrils and sarcoplasmic reticulum. This study demonstrates that all the characteristic organelles of mature skeletal muscle can develop in vitro in the absence of nerves.

Creatine kinase and aldolase isoenzyme transitions in cultures of chick skeletal muscle cells

1974 ◽  
Vol 37 (1) ◽  
pp. 63-89 ◽  
Author(s):  
David C. Turner ◽  
Vreni Maier ◽  
Hans M. Eppenberger
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

Diaphragm tension reduced in dystrophic mice by an oxidant, hypochlorous acid

2010 ◽  
Vol 88 (2) ◽  
pp. 130-140
Author(s):  
Aude Lafoux ◽  
Alexandra Divet ◽  
Pascal Gervier ◽  
Corinne Huchet-Cadiou
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Hypochlorous Acid ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Diaphragm Muscle ◽  
Mdx Mouse ◽  
Mdx Mice ◽  
Skinned Fibres ◽  
Dystrophic Mice

In dystrophin-deficient skeletal muscle cells, in which Ca2+ homeostasis is disrupted and reactive oxygen species production is increased, we hypothesized that hypochlorous acid (HOCl), a strong H2O2-related free radical, damages contractile proteins and the sarcoplasmic reticulum. The aim of the present study was to investigate the effects of exposure to oxidative stress, generated by applying HOCl (100 µmol/L and 1 mmol/L), on the contractile function and sarcoplasmic reticulum properties of dystrophic mice. Experiments were performed on diaphragm muscle, which is severely affected in the mdx mouse, and the results were compared with those obtained in healthy (non-dystrophic) mice. In Triton-skinned fibres from C57BL/10 and mdx mice, 1 mmol/L HOCl increased myofibrillar Ca2+ sensitivity, but decreased maximal Ca2+-activated tension. In the presence of HOCl, higher concentrations of MgATP were required to produce rigor tensions. The interaction between HOCl and the Ca2+ uptake mechanisms was demonstrated using saponin-skinned fibres and sarcoplasmic reticulum vesicles. The results showed that HOCl, at micromolar or millimolar concentrations, can modify sarcoplasmic reticulum Ca2+ uptake and that this effect was more pronounced in diaphragm muscle from mdx mice. We conclude that in dystrophic diaphragm skeletal muscle cells, HOCl activates a cellular pathway that leads to an increase in the intracellular concentration of Ca2+.

scholarly journals Monosodium Iodoacetate delays regeneration and inhibits hypertrophy in skeletal muscle cells in vitro

2019 ◽  
Author(s):  
Rowan P. Rimington ◽  
Darren J. Player ◽  
Neil R.W. Martin ◽  
Mark P. Lewis
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cells ◽  
Rodent Model ◽  
Skeletal Muscle Cells ◽  
Skeletal Muscle Regeneration ◽  
Index Number ◽  
Monosodium Iodoacetate ◽  
The Impact

AbstractObjectiveOsteoarthritis (OA) is a musculoskeletal disease which contributes to severe morbidity. The monosodium iodoacetate (MIA) rodent model of OA is now well established, however the effect of MIA on surrounding tissues post injection has not been investigated and as such the impact on phenotypic development is unknown. The aim of this investigation was to examine the impact of MIA incubation on skeletal muscle cells in vitro, to provide an indication as to the potential influence of MIA administration of skeletal muscle in vivo.MethodsC2C12 skeletal muscle myotubes were treated with either 4.8μM MIA or 10μM Dexamethasone (DEX, positive atrophic control) up to 72hrs post differentiation and sampled for morphological and mRNA analyses.ResultsSignificant morphological effects (fusion index, number of myotubes and myotube width, p<0.05) were evident, demonstrating a hypertrophic phenotype in control (CON) compared to a hyperplasic phenotype in MIA and DEX. Increases in MAFbx mRNA were also evident between conditions, with post-hoc analysis demonstrating significance between CON and DEX (p<0.001), but not between CON and MIA (p>0.05).ConclusionsThese data indicate a significant impact of both DEX and MIA on regeneration and hypertrophy in vitro and suggest differential activating mechanisms. Future investigations should determine whether skeletal muscle regeneration and hypertrophy is affected in the in vivo rodent model and the potential impact this has on the OA phenotypic outcome.

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