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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Autophagic-lysosomal pathway functions in the masseter and tongue muscles in the klotho mouse, a mouse model for aging.
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Autophagic-lysosomal pathway functions in the masseter and tongue muscles in the klotho mouse, a mouse model for aging.

机译：自噬溶酶体途径在klotho小鼠（一种衰老的小鼠模型）的咬肌和舌头肌肉中起作用。

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摘要

Klotho mutant (kl/kl) mice, a type of short-lived mouse models, display several aging-related phenotypes. To investigate whether the atrophy of skeletal muscles is induced in these mice via activation of the ubiquitin-proteasomal pathway and/or the autophagic-lysosomal pathway through an alteration of insulin/IGF-I signaling, we analyzed the activity of the two pathways for protein degradation and components of the insulin/IGF signaling pathway in their skeletal muscles. The masseter, tongue, and gastrocnemius muscles in kl/kl showed marked reductions in muscle weight and in myofiber diameter compared with +/+. The autophagic-lysosomal pathway in kl/kl was activated in the masseter and tongue, but not in the gastrocnemius, compared with that in +/+, whereas the ubiquitin-proteasomal pathway in these three muscles of kl/kl was not altered. No marked difference in the phosphorylation levels of insulin/IGF-I signaling components, such as insulin/IGF-I receptor, Akt, and FoxO in three muscles studied were found between kl/kl and +/+, but the phosphorylation levels of signaling component at the downstream of mTOR such as 4E-BP1 and p70 S6K were suppressed in the masseter and tongue of kl/kl compared with +/+. Deficiency of essential amino acids is reported to activate the autophagy-lysosomal pathway through the down-regulation of mTOR, not through IGF-Akt-FoxO. The masseter and tongue seem to be more actively moved than limb muscles in kl/kl, because they are essential for survival activities such as mastication, swallowing, and respiration. Thus, the deficiency of amino acid by the active movement of the masseter and tongue seems to stimulate the autophagic-lysosomal pathway via the down-regulation of mTOR signalling pathway.
机译：Klotho突变（kl / kl）小鼠是一种短寿命的小鼠模型，具有几种衰老相关的表型。为了研究是否通过激活胰岛素/ IGF-I信号转导的泛素-蛋白酶体途径和/或自噬-溶酶体途径在这些小鼠中诱导骨骼肌萎缩，我们分析了两种途径的蛋白质活性骨骼肌中胰岛素/ IGF信号通路的降解和组成。与+ / +相比，kl / kl中的咬肌，舌头和腓肠肌的肌肉重量和肌纤维直径明显减少。与+ / +相比，kl / kl中的自噬溶酶体途径在咬肌和舌头中被激活，而腓肠肌中未被激活，而在kl / kl的这三处肌肉中的泛素-蛋白酶体途径没有改变。在kl / kl和+ / +之间没有发现胰岛素/ IGF-1信号传导成分（如胰岛素/ IGF-1受体，Akt和FoxO）的磷酸化水平有明显差异，但信号传导的磷酸化水平与+ / +相比，mTOR下游的咬肌和舌头中的mTOR成分（例如4E-BP1和p70 S6K）受到抑制。据报道，必需氨基酸的缺乏会通过下调mTOR而不是通过IGF-Akt-FoxO激活自噬-溶酶体途径。在kl / kl中，咬肌和舌头似乎比肢体肌肉更活跃，因为它们对于诸如咀嚼，吞咽和呼吸等生存活动至关重要。因此，由咬肌和舌头的主动运动引起的氨基酸缺乏似乎通过下调mTOR信号传导途径刺激自噬-溶酶体途径。

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