重症肌无力患者骨骼肌内质网伴侣蛋白GRP78表达增加。
Increased skeletal muscle expression of the endoplasmic reticulum chaperone GRP78 in patients with myasthenia gravis.
作者信息
Iwasa Kazuo, Nambu Yoshinori, Motozaki Yuko, Furukawa Yutaka, Yoshikawa Hiroaki, Yamada Masahito
机构信息
Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, 13-1 Takara-Machi, Kanazawa 920-8640, Japan.
Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, 13-1 Takara-Machi, Kanazawa 920-8640, Japan.
出版信息
J Neuroimmunol. 2014 Aug 15;273(1-2):72-6. doi: 10.1016/j.jneuroim.2014.05.006. Epub 2014 May 21.
In myasthenia gravis (MG), damage to neuromuscular junctions may induce endoplasmic reticulum (ER) stress in skeletal muscles. In the current study, skeletal muscles obtained from patients with MG exhibited upregulation of glucose-regulated protein 78 (GRP78) mRNA that was activated by ER stress. Furthermore, GRP78 mRNA expression was higher in patients with MG and myositis than in patients with non-myopathy. We also observed a significant positive correlation between GRP78 mRNA expression and GRP78 protein levels and between GRP78 mRNA expression and age of MG onset. Our findings suggest that muscle weakness in MG might be caused by both neuromuscular junction disruption and ER stress.
在重症肌无力（MG）中，神经肌肉接头损伤可能会诱导骨骼肌中的内质网（ER）应激。在当前研究中，从MG患者获取的骨骼肌显示出由ER应激激活的葡萄糖调节蛋白78（GRP78）mRNA上调。此外，MG和肌炎患者的GRP78 mRNA表达高于非肌病患者。我们还观察到GRP78 mRNA表达与GRP78蛋白水平之间以及GRP78 mRNA表达与MG发病年龄之间存在显著正相关。我们的研究结果表明，MG中的肌肉无力可能是由神经肌肉接头破坏和ER应激共同引起的。
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