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首页> 外文期刊>Journal of Cellular Physiology >The metabolic and molecular mechanisms of hyperammonaemia‐ and hyperethanolaemia‐induced protein catabolism in skeletal muscle cells
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The metabolic and molecular mechanisms of hyperammonaemia‐ and hyperethanolaemia‐induced protein catabolism in skeletal muscle cells

机译：的代谢和分子机制hyperammonaemia》hyperethanolaemia诱导在骨骼肌细胞蛋白质分解代谢

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Hyperammonaemia and hyperethanolaemia are thought to be driving factors behind skeletal muscle myopathy in liver disease, that is, cirrhosis. Despite this, the singular and combined impacts of ethanol‐ and ammonia‐induced protein catabolism are poorly defined. As such, we aimed to dissect out the effects of ammonia and ethanol on muscle catabolism. Murine C2C12 myotubes were treated with ammonium acetate (10?mM) and ethanol (100?mM) either alone or in combination for 4?hr and/or 24?hr. Myotube diameter, muscle protein synthesis and anabolic and catabolic signalling pathways were assessed. In separate experiments, cells were cotreated with selected inhibitors of protein breakdown to assess the importance of proteolytic pathways in protein loss with ammonia and ethanol. Ammonia and ethanol in combination resulted in a reduction in myotube width and total protein content, which was greater than the reduction observed with ammonia alone. Both ammonia and ethanol caused reductions in protein synthesis, as assessed by puromycin incorporation. There was also evidence of impairments in regulation of protein translation, and increased protein expression of markers of muscle protein breakdown. Myotube protein loss with ammonia plus ethanol was not affected by autophagy inhibition, but was completely prevented by proteasome inhibition. Thus, combined ammonia and ethanol incubation of C2C12 myotubes exacerbated myotube atrophy and dysregulation of anabolic and catabolic signalling pathways associated with either component individually. Ubiquitin proteasome‐mediated protein breakdown appears to play an important role in myotube protein loss with ethanol and ammonia.
机译：Hyperammonaemia和hyperethanolaemia思想骨骼肌背后的驱动因素肌病在肝脏疾病,肝硬化。尽管如此,奇异和组合的影响乙醇的量和氨检测诱导蛋白质定义糟糕的分解代谢。解剖出氨和乙醇的影响对肌肉分解代谢。醋酸铵处理(10 ?毫米)和乙醇(100 ?毫米)单独或组合4 ?和/或24 ?人力资源。合成和合成代谢和分解代谢的信号途径进行了评估。细胞被cotreated与选定的抑制剂蛋白质分解评估的重要性蛋白水解途径与氨蛋白质损失和乙醇。导致肌管宽度和的减少总蛋白质含量大于减少观察与氨。氨和乙醇减少蛋白质引起的嘌呤霉素合成,作为评估合并。监管障碍的蛋白质翻译、和标记的蛋白表达增加肌肉蛋白质分解。与氨+乙醇并没有受到影响自噬抑制,但完全预防由蛋白酶体抑制。结合氨和乙醇C2C12孵化肌管加重肌小管萎缩合成代谢和分解代谢的调节异常相关信号通路单独的组件。蛋白酶体介导的蛋白质分解似乎发挥重要作用肌管蛋白质损失与乙醇和氨。

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