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Regulation of Contractile Proteins and Protein Translational Signaling in Disused Muscle

机译：废弃肌肉中收缩蛋白的调节和蛋白翻译信号

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Background/Aims: Muscle disuse can lead to muscle atrophy and impaired skeletal muscle function. How skeletal muscle modulates protein translational signaling in response to prolonged muscle disuse is not well understood. Using the hindlimb unloading (HU) model of muscle atrophy we examined how hindlimb unweighting affects protein translational signaling, including the activation of Akt/mTOR/p70S6K/S6 signaling and the inhibitory association of 4EBP1 with translation initiation factor eIF4E. Methods: Male F344BN rats were randomized into baseline control, or subjected to HU for 3, 7 or 14 days. Body weight, gastrocnemius muscle, and individual myofiber cross-sectional area were measured to evaluate the degree of muscle atrophy. The amounts of myosin and related muscle contractile proteins were assessed using SDS-PAGE and immunoblotting. Microarray analysis was used to evaluate changes in the mRNA expression of muscle contractile proteins. Total and phosphorylated proteins of Akt/mTOR/p70S6K/S6 pathway were determined via immunoblotting, while the association of 4EBP1 with eIF4E was detected via co-immunoprecipitation. Results: Unloading for 3 days significantly reduced cytosolic myosin content and was associated with increased binding of 4EBP1 to eIF4E, while prolonged unloading (14 days) was associated with the activation of Akt/mTOR/p70S6K/S6 signaling, decreased binding of 4EBP1 to eIF4E, increased cytosolic myosin and elevations in myofibrillar mRNA levels. Conclusion: Taken together, these data suggest that prolonged muscle disuse induces a biphasic translational signaling response that is associated with diminished and then increased muscle contractile protein expression.
机译：背景/目的：肌肉废用可导致肌肉萎缩和骨骼肌功能受损。骨骼肌如何响应长时间的肌肉废用而调节蛋白质翻译信号转导尚不清楚。使用肌肉萎缩的后肢卸载（HU）模型，我们检查了后肢未加权如何影响蛋白质翻译信号传导，包括Akt / mTOR / p70S6K / S6信号传导的激活以及4EBP1与翻译起始因子eIF4E的抑制性关联。方法：将雄性F344BN大鼠随机分为基线对照组，或接受HU治疗3、7或14天。测量体重，腓肠肌和单个肌纤维横截面积以评估肌肉萎缩的程度。使用SDS-PAGE和免疫印迹评估肌球蛋白和相关肌肉收缩蛋白的量。微阵列分析被用来评估肌肉收缩蛋白的mRNA表达的变化。通过免疫印迹确定Akt / mTOR / p70S6K / S6途径的总蛋白和磷酸化蛋白，而通过共免疫沉淀检测4EBP1与eIF4E的关联。结果：卸载3天可显着降低胞质肌球蛋白含量，并与增加4EBP1与eIF4E的结合有关，而延长卸载（14天）与激活Akt / mTOR / p70S6K / S6信号有关，降低4EBP1与eIF4E的结合，胞质肌球蛋白增加和肌原纤维mRNA水平升高。结论：综上所述，这些数据表明延长的肌肉废用诱导了双相翻译信号传导反应，该反应与肌肉收缩蛋白表达降低然后升高有关。

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