scholarly journals Influence of the PDE5 inhibitor tadalafil on redox status and antioxidant defense system in C2C12 skeletal muscle cells

2017 ◽  
Vol 22 (3) ◽  
pp. 389-396 ◽  
Author(s):  
Guglielmo Duranti ◽  
Roberta Ceci ◽  
Paolo Sgrò ◽  
Stefania Sabatini ◽  
Luigi Di Luigi
Keyword(s):  
Skeletal Muscle ◽  
Antioxidant Defense ◽  
Pde5 Inhibitor ◽  
Muscle Cells ◽  
Antioxidant Defense System ◽  
Redox Status ◽  
Skeletal Muscle Cells ◽  
Defense System ◽  
C2c12 Skeletal Muscle Cells

scholarly journals Proliferative effect of Hachimijiogan, a Japanese herbal medicine, in C2C12 skeletal muscle cells

Maturitas ◽  
2015 ◽  
Vol 81 (1) ◽  
pp. 231
Author(s):  
Takashi Takeda ◽  
Kenji Tsuiji ◽  
Bin Li ◽  
Mari Tadakawa ◽  
Masami Shiina ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Herbal Medicine ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Proliferative Effect ◽  
Japanese Herbal Medicine ◽  
C2c12 Skeletal Muscle Cells

Skeletal muscle uncoupling-induced longevity in mice is linked to increased substrate metabolism and induction of the endogenous antioxidant defense system

2013 ◽  
Vol 304 (5) ◽  
pp. E495-E506 ◽  
Author(s):  
S. Keipert ◽  
M. Ost ◽  
A. Chadt ◽  
A. Voigt ◽  
V. Ayala ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Mapk Signaling ◽  
Redox Signaling ◽  
Defense System ◽  
High Fat ◽  
Substrate Metabolism ◽  
Endogenous Antioxidant

Ectopic expression of uncoupling protein 1 (UCP1) in skeletal muscle (SM) mitochondria increases lifespan considerably in high-fat diet-fed UCP1 Tg mice compared with wild types (WT). To clarify the underlying mechanisms, we investigated substrate metabolism as well as oxidative stress damage and antioxidant defense in SM of low-fat- and high-fat-fed mice. Tg mice showed an increased protein expression of phosphorylated AMP-activated protein kinase, markers of lipid turnover (p-ACC, FAT/CD36), and an increased SM ex vivo fatty acid oxidation. Surprisingly, UCP1 Tg mice showed elevated lipid peroxidative protein modifications with no changes in glycoxidation or direct protein oxidation. This was paralleled by an induction of catalase and superoxide dismutase activity, an increased redox signaling (MAPK signaling pathway), and increased expression of stress-protective heat shock protein 25. We conclude that increased skeletal muscle mitochondrial uncoupling in vivo does not reduce the oxidative stress status in the muscle cell. Moreover, it increases lipid metabolism and reactive lipid-derived carbonyls. This stress induction in turn increases the endogenous antioxidant defense system and redox signaling. Altogether, our data argue for an adaptive role of reactive species as essential signaling molecules for health and longevity.

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.

Dreh, a long noncoding RNA repressed by metformin, regulates glucose transport in C2C12 skeletal muscle cells

Life Sciences ◽  
2019 ◽  
Vol 236 ◽  
pp. 116906 ◽  
Author(s):  
Nobuhiko Takahashi ◽  
Atsushi P. Kimura ◽  
Kai Otsuka ◽  
Kazumasa Ohmura ◽  
Sumiyoshi Naito ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
C2c12 Skeletal Muscle Cells

scholarly journals Zinc Modulates Several Transcription-Factor Regulated Pathways in Mouse Skeletal Muscle Cells

Molecules ◽  
2020 ◽  
Vol 25 (21) ◽  
pp. 5098
Author(s):  
Parisa Vahidi Ferdowsi ◽  
Rachel Ng ◽  
John Adulcikas ◽  
Sukhwinder Singh Sohal ◽  
Stephen Myers
Keyword(s):  
Skeletal Muscle ◽  
Transcription Factor ◽  
Metal Ion ◽  
Insulin Signalling ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Western Blots ◽  
Insulin Signalling Pathway ◽  
C2c12 Skeletal Muscle Cells

Zinc is an essential metal ion involved in many biological processes. Studies have shown that zinc can activate several molecules in the insulin signalling pathway and the concomitant uptake of glucose in skeletal muscle cells. However, there is limited information on other potential pathways that zinc can activate in skeletal muscle. Accordingly, this study aimed to identify other zinc-activating pathways in skeletal muscle cells to further delineate the role of this metal ion in cellular processes. Mouse C2C12 skeletal muscle cells were treated with insulin (10 nM), zinc (20 µM), and the zinc chelator TPEN (various concentrations) over 60 min. Western blots were performed for the zinc-activation of pAkt, pErk, and pCreb. A Cignal 45-Reporter Array that targets 45 signalling pathways was utilised to test the ability of zinc to activate pathways that have not yet been described. Zinc and insulin activated pAkt over 60 min as expected. Moreover, the treatment of C2C12 skeletal muscle cells with TPEN reduced the ability of zinc to activate pAkt and pErk. Zinc also activated several associated novel transcription factor pathways including Nrf1/Nrf2, ATF6, CREB, EGR1, STAT1, AP-1, PPAR, and TCF/LEF, and pCREB protein over 120 min of zinc treatment. These studies have shown that zinc’s activity extends beyond that of insulin signalling and plays a role in modulating novel transcription factor activated pathways. Further studies to determine the exact role of zinc in the activation of transcription factor pathways will provide novel insights into this metal ion actions.

scholarly journals Caffeine Affects Myotube Size As Well As Regulates Protein Degradation and Protein Synthesis Pathways in C2C12 Skeletal Muscle Cells

2016 ◽  
Vol 6 (2) ◽  
pp. 88-96 ◽  
Author(s):  
Tatsuro Egawa ◽  
Yoshitaka Ohno ◽  
Ayumi Goto ◽  
Takao Sugiura ◽  
Yoshinobu Ohira ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Protein Degradation ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
C2c12 Skeletal Muscle Cells
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