l-Carnitine: a potential treatment for blocking apoptosis and preventing skeletal muscle myopathy in heart failure

2002 ◽  
Vol 283 (3) ◽  
pp. C802-C810 ◽  
Author(s):  
Giorgio Vescovo ◽  
Barbara Ravara ◽  
Valerio Gobbo ◽  
Marco Sandri ◽  
Annalisa Angelini ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Congestive Heart Failure ◽  
Muscle Metabolism ◽  
Muscle Cells ◽  
Serum Levels ◽  
Skeletal Muscle Cells ◽  
Tnf Α ◽  
Factor Α

Skeletal muscle in congestive heart failure is responsible for increased fatigability and decreased exercise capacity. A specific myopathy with increased expression of fast-type myosins, myocyte atrophy, secondary to myocyte apoptosis triggered by high levels of circulating tumor necrosis factor-α (TNF-α) has been described. In an animal model of heart failure, the monocrotaline-treated rat, we have observed an increase of apoptotic skeletal muscle nuclei. Proapoptotic agents, caspase-3 and -9, were increased, as well as serum levels of TNF-α and its second messenger sphingosine. Treatment of rats withl-carnitine, known for its protective effect on muscle metabolism injuries, was found to inhibit caspases and to decrease the levels of TNF-α and sphingosine, as well as the number of apoptotic myonuclei. Staurosporine was used in in vitro experiments to induce apoptosis in skeletal muscle cells in culture. Whenl-carnitine was applied to skeletal muscle cells, before staurosporine treatment, we observed a reduction in apoptosis. These findings show that l-carnitine can prevent apoptosis of skeletal muscles cells and has a role in the treatment of congestive heart failure-associated myopathy.

In Vitro Effects of Soy Phytoestrogens on Rat L6 Skeletal Muscle Cells

2005 ◽  
Vol 8 (3) ◽  
pp. 327-331 ◽  
Author(s):  
K.L. Jones ◽  
J. Harty ◽  
M.J. Roeder ◽  
T.A. Winters ◽  
W.J. Banz
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
In Vitro Effects ◽  
L6 Skeletal Muscle Cells

Characterization of β-adrenoceptors on rat skeletal muscle cells grown in vitro

1990 ◽  
Vol 40 (5) ◽  
pp. 1043-1048 ◽  
Author(s):  
Marie-Helene Disatnik ◽  
Sanford R. Sampson ◽  
Asher Shainberg
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Rat Skeletal Muscle

scholarly journals Hyaluronic acid levels are increased in complicated parapneumonic pleural effusions

2015 ◽  
Vol 75 (3) ◽  
Author(s):  
T. Zaga ◽  
D. Makris ◽  
I. Tsilioni ◽  
T. Kiropoulos ◽  
S. Oikonomidi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Extracellular Matrix ◽  
Congestive Heart Failure ◽  
Hyaluronic Acid ◽  
Pleural Fluid ◽  
Inflammatory Process ◽  
Serum Levels ◽  
Pleural Effusions ◽  
Tnf Α ◽  
Malignant Effusions

Background and Aim. Hyaluronic acid (HA) is a component of extracellular matrix and may play a role in the pleural inflammation which is implicated in parapneumonic effusions.The aim of the current study was to investigate HA levels in serum and pleura in patients with parapneumonic effusions. Methods. We prospectively studied pleural and serum levels of HA in 58 patients with pleural effusions due to infection (complicated and uncomplicated parapneumonic effusions), malignant effusions and transudative effusions due to congestive heart failure. In addition to HA, TNF-α and IL-1β levels were determined in pleural fluid and serum by ELISA. Results. The median±SD HA levels (pg/ml) in pleural fluid of patients with complicated effusions (39.058±11.208) were significantly increased (p<0.005), compared to those with uncomplicated parapneumonic effusions (11.230±1.969), malignant effusions (10.837±4.803) or congestive heart failure (5.392±3.133). There was no correlation between pleural fluid and serum HA values. Pleural fluid TNF-α levels (146±127 pg/mL) and IL-1β levels (133.4±156 pg/mL) were significantly higher in patients with complicated parapneumonic effusions compared to patients with other types of effusion (p<0.05). No significant association between HA and TNF-α or IL-1β was found. Conclusions. HA may play a significant role in the inflammatory process which characterises exudative infectious pleuritis. Further investigation might reveal whether HA is a useful marker in the management of parapneumonic effusions.

scholarly journals Palmitate Induces Tumor Necrosis Factor-α Expression in C2C12 Skeletal Muscle Cells by a Mechanism Involving Protein Kinase C and Nuclear Factor-κB Activation

Endocrinology ◽  
2006 ◽  
Vol 147 (1) ◽  
pp. 552-561 ◽  
Author(s):  
Mireia Jové ◽  
Anna Planavila ◽  
Rosa M. Sánchez ◽  
Manuel Merlos ◽  
Juan Carlos Laguna ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase C ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Mrna Levels ◽  
Nuclear Factor ◽  
Kinase C ◽  
Tnf Α ◽  
Fold Induction ◽  
C2c12 Skeletal Muscle Cells

The mechanisms responsible for increased expression of TNF-α in skeletal muscle cells in diabetic states are not well understood. We examined the effects of the saturated acid palmitate on TNF-α expression. Exposure of C2C12 skeletal muscle cells to 0.75 mm palmitate enhanced mRNA (25-fold induction, P < 0.001) and protein (2.5-fold induction) expression of the proinflammatory cytokine TNF-α. This induction was inversely correlated with a fall in GLUT4 mRNA levels (57% reduction, P < 0.001) and glucose uptake (34% reduction, P < 0.001). PD98059 and U0126, inhibitors of the ERK-MAPK cascade, partially prevented the palmitate-induced TNF-α expression. Palmitate increased nuclear factor (NF)-κB activation and incubation of the cells with the NF-κB inhibitors pyrrolidine dithiocarbamate and parthenolide partially prevented TNF-α expression. Incubation of palmitate-treated cells with calphostin C, a strong and specific inhibitor of protein kinase C (PKC), abolished palmitate-induced TNF-α expression, and restored GLUT4 mRNA levels. Palmitate treatment enhanced the expression of phospho-PKCθ, suggesting that this PKC isoform was involved in the changes reported, and coincubation of palmitate-treated cells with the PKC inhibitor chelerythrine prevented the palmitate-induced reduction in the expression of IκBα and insulin-stimulated Akt activation. These findings suggest that enhanced TNF-α expression and GLUT4 down-regulation caused by palmitate are mediated through the PKC activation, confirming that this enzyme may be a target for either the prevention or the treatment of fatty acid-induced insulin resistance.

scholarly journals Interaction and cystogenesis of Toxoplasma gondii within skeletal muscle cells in vitro

2009 ◽  
Vol 104 (2) ◽  
pp. 170-174 ◽  
Author(s):  
Erick Vaz Guimarães ◽  
Laís de Carvalho ◽  
Helene Santos Barbosa
Keyword(s):  
Skeletal Muscle ◽  
Toxoplasma Gondii ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

scholarly journals Silk fibroin scaffolds with muscle-like elasticity support in vitro differentiation of human skeletal muscle cells

2016 ◽  
Vol 11 (11) ◽  
pp. 3178-3192 ◽  
Author(s):  
Vishal Chaturvedi ◽  
Deboki Naskar ◽  
Beverley F. Kinnear ◽  
Elizabeth Grenik ◽  
Danielle E. Dye ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Silk Fibroin ◽  
Human Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
In Vitro Differentiation ◽  
Human Skeletal Muscle Cells
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