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首页> 外文期刊>Journal of Cellular Physiology >TWEAK causes myotube atrophy through coordinated activation of ubiquitin-proteasome system, autophagy, and caspases
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TWEAK causes myotube atrophy through coordinated activation of ubiquitin-proteasome system, autophagy, and caspases

机译：通过协调调整导致肌小管萎缩ubiquitin-proteasome系统的激活,还存在自噬,

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摘要

Proinflammatory cytokine TWEAK has now emerged as a key mediator of skeletal muscle-wasting in many catabolic conditions. However, the mechanisms by which TWEAK induces muscle proteolysis remain poorly understood. Here, we have investigated the role of ubiquitin-proteasome system, autophagy, and caspases in TWEAK-induced muscle wasting. Addition of TWEAK to C2C12 myotubes stimulated the ubiquitination of myosin heavy chain (MyHC) and augmented the expression of E3 ubiquitin ligase MuRF1. Pretreatment of myotubes with proteasome inhibitors MG132 or lactacystin or knockdown of MuRF1 by RNAi blocked the TWEAK-induced degradation of MyHC and myotube atrophy. TWEAK increased the expression of several autophagy-related molecules. Moreover, the inhibitors of autophagy improved the levels of MyHC in TWEAK-treated myotubes. TWEAK also increased activity of caspases in C2C12 myotubes. Pan-caspase or caspase 3 inhibitory peptide inhibited the TWEAK-induced loss of MyHC and myotube diameter. Our study demonstrates that nuclear factor-kappa B (NF-κB) transcription factor is essential for TWEAK-induced expression of MuRF1 and Beclin1. Furthermore, our results suggest that caspases contribute, at least in part, to the activation of NF-κB in response to TWEAK treatment. Collectively, the present study provides novel insight into the mechanisms of action of TWEAK in skeletal muscle.
机译：促炎细胞因子调整已经成为骨骼肌肉的关键中介在许多分解代谢的条件。调整诱发肌肉蛋白水解作用保持知之甚少。ubiquitin-proteasome系统的作用,自噬,和还在TWEAK-induced肌肉萎缩。增加调整C2C12肌管的刺激肌凝蛋白重链的泛素化(MyHC)和增强E3泛素的表达连接酶MuRF1。蛋白酶体抑制剂MG132 lactacystin或可拆卸的MuRF1 RNAi封锁了TWEAK-induced MyHC退化和肌管萎缩。几个autophagy-related分子。自噬抑制剂改善水平的MyHC TWEAK-treated肌管。增加的活动还在C2C12肌管。Pan-caspase或半胱天冬酶3抑制肽抑制了TWEAK-induced MyHC和损失肌管直径。核factor-kappa B (NF -κB)转录因素对TWEAK-induced表达至关重要MuRF1 Beclin1。表明还存在贡献,至少在部分,NF -κB的活化反应调整治疗。提供了新的见解的机制行动在骨骼肌的调整。

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