scholarly journals GH Regulation of IGF-I and Suppressor of Cytokine Signaling Gene Expression in C2C12 Skeletal Muscle Cells

Endocrinology ◽  
2001 ◽  
Vol 142 (9) ◽  
pp. 3890-3900 ◽  
Author(s):  
Cynthia L. Sadowski ◽  
Thomas T. Wheeler ◽  
Lu-Hai Wang ◽  
Henry B. Sadowski
2012 ◽  
Vol 373 (1-2) ◽  
pp. 107-113 ◽  
Author(s):  
Shuang Jiao ◽  
Hongxia Ren ◽  
Yun Li ◽  
Jianfeng Zhou ◽  
Cunming Duan ◽  
...  

2021 ◽  
Vol 11 (5) ◽  
pp. 2272
Author(s):  
Mansour Haddad

Background: Adenosine plays the role of regulating cell differentiation, proliferation, and apoptosis in various kinds of cells through the B-cell lymphoma 2 (BCL2) pathway. Objectives: Since anti-apoptotic (BCL2) expression plays a role in controlling apoptosis in some cell lines, this study was designed to investigate whether adenosine analogue, NECA (non-selective adenosine receptors agonist), selective adenosine A2B receptor antagonist, PSB 603, and a selective adenosine A2A receptor agonist, CG21680, affect BCL2-gene expression in the skeletal muscle cells of rats. The purpose of this investigation was to test the hypothesis that CG21680 treatment would significantly intensify BCL2 gene expression in rat skeletal muscle. Methods: Flasks measuring 25 cm2 were employed in culturing the rat L6 skeletal muscle cells. After treating these differential cells, the relative mRNA expression level for the BCL2 gene, at varying conditions of treatment, was measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Results: From the qRT-PCR analysis results, it was concluded that BCL2 expression was markedly amplified after selective adenosine A2A receptor agonist, CGS21680 (p < 0.01) treatment. More prospective validation for the adenosine receptors’ contribution in modulating apoptosis by NECA was delivered by the outcomes from the combined pre-treatment of the cells with NECA and PSB 603. These outcomes show that when starved skeletal muscle cells are treated with a combination of NECA and 100 nM PSB 603, there was a substantial decrease in comparison to either treatment used on its own. Conclusions: This study’s results showed, for the first time, an increase in BCL2 gene expression within skeletal muscle after CGS21680 treatment. Hence, the prospective escalation in BCL2 protein expression might have a protective role to play against apoptosis and avert damage to the skeletal muscle.


Maturitas ◽  
2015 ◽  
Vol 81 (1) ◽  
pp. 231
Author(s):  
Takashi Takeda ◽  
Kenji Tsuiji ◽  
Bin Li ◽  
Mari Tadakawa ◽  
Masami Shiina ◽  
...  

Endocrinology ◽  
2006 ◽  
Vol 147 (1) ◽  
pp. 552-561 ◽  
Author(s):  
Mireia Jové ◽  
Anna Planavila ◽  
Rosa M. Sánchez ◽  
Manuel Merlos ◽  
Juan Carlos Laguna ◽  
...  

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 &lt; 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 &lt; 0.001) and glucose uptake (34% reduction, P &lt; 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.


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