Autophagy under glucose starvation enhances protein translation initiation in response to re-addition of glucose in C2C12 myotubes.,FEBS Open Bio

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Autophagy under glucose starvation enhances protein translation initiation in response to re-addition of glucose in C2C12 myotubes.
FEBS Open Bio ( IF 2.8 ) Pub Date : 2020-09-03 , DOI: 10.1002/2211-5463.12970
Naoya Nakai ₁ , Saki Kitai ₁ , Noriko Iida ₁ , Sachika Inoue ₁ , Kazuhiko Higashida ₁

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Proteolysis is known to play a crucial role in maintaining skeletal muscle mass and function. Autophagy is a conserved intracellular process for the bulk degradation of proteins in lysosomes. Although nutrient starvation is known to induce autophagy, the effect of nutrient repletion following starvation on the mTOR pathway‐mediated protein translation remains unclear. In the present study, we examined the effect of glucose starvation on the initiation of protein translation in response to glucose re‐addition in C2C12 myotubes. Glucose starvation decreased the phosphorylation of p70 S6 kinase (p70S6K), a bonafide marker for protein translation initiation. Following re‐addition of glucose, phosphorylation of p70S6K markedly increased only in glucose‐starved cells. Inhibiting autophagy using pharmacological inhibitors diminished the effect of glucose re‐addition on the phosphorylation of p70S6K, whereas inhibition of the ubiquitin‐proteasome system did not exert any effect. In conclusion, autophagy under glucose starvation partially accounts for the activation of translation initiation by re‐addition of glucose.

中文翻译：

葡萄糖饥饿下的自噬增强了响应于 C2C12 肌管中重新添加葡萄糖的蛋白质翻译起始。

已知蛋白水解在维持骨骼肌质量和功能方面起着至关重要的作用。自噬是溶酶体中蛋白质大量降解的保守细胞内过程。尽管已知营养缺乏会诱导自噬，但饥饿后营养补充对 mTOR 通路介导的蛋白质翻译的影响仍不清楚。在本研究中，我们检查了葡萄糖饥饿对响应于 C2C12 肌管中葡萄糖再添加而启动蛋白质翻译的影响。葡萄糖饥饿降低了 p70 S6 激酶 (p70S6K) 的磷酸化，p70 S6 激酶是蛋白质翻译起始的真正标志物。重新加入葡萄糖后，p70S6K 的磷酸化仅在葡萄糖饥饿的细胞中显着增加。使用药理学抑制剂抑制自噬降低了葡萄糖再添加对 p70S6K 磷酸化的影响，而抑制泛素-蛋白酶体系统则没有任何作用。总之，葡萄糖饥饿下的自噬部分解释了通过重新添加葡萄糖来激活翻译起始。

更新日期：2020-10-02

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