Increased skeletal muscle expression of the endoplasmic reticulum chaperone GRP78 in patients with myasthenia gravis

被引：15
|
作者：
Iwasa, Kazuo [1 ]
Nambu, Yoshinori [1 ]
Motozaki, Yuko [2 ]
Furukawa, Yutaka [3 ]
Yoshikawa, Hiroaki [4 ]
Yamada, Masahito [1 ]
机构：
[1] Kanazawa Univ, Grad Sch Med Sci, Dept Neurol & Neurobiol Aging, Kanazawa, Ishikawa 9208640, Japan
[2] Iou Natl Hosp, Dept Neurol, Kanazawa, Ishikawa 9200192, Japan
[3] Takaoka Koseiren Hosp, Dept Neurol, Takaoka, Toyama 9338555, Japan
[4] Kanazawa Univ, Hlth Serv Ctr, Kanazawa, Ishikawa 9201192, Japan
来源：
JOURNAL OF NEUROIMMUNOLOGY | 2014年 / 273卷 / 1-2期
关键词：
Myasthenia gravis; Endoplasmic reticulum (ER) stress response; Glucose-regulated protein 78 (GRP78); Skeletal muscle; UNFOLDED PROTEIN RESPONSE; RECEPTOR ANTIBODIES; STRESS; AUTOANTIBODIES; CELLS; MYOSITIS;
D O I：
10.1016/j.jneuroim.2014.05.006
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
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. (C)2014 Elsevier B.V. All rights reserved.
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页码：72 / 76
页数：5
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