Overexpression of GRP78 protects glial cells from endoplasmic reticulum stress
Overexpression of GRP78 protects glial cells from endoplasmic reticulum stress
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DOI：
10.1016/j.neulet.2011.09.045
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发表时间：
2011-10-31
影响因子：
2.5
通讯作者：
Mochida, Joji
中科院分区：
文献类型：
--
作者：
Suyama, Kaori;Watanabe, Masahiko;Mochida, Joji
内质网（ER）应激通过引起结构异常蛋白的积累诱导凋亡性细胞死亡。78-kDa葡萄糖调节蛋白（GRP 78）是一种ER伴侣蛋白，可调节ER中的蛋白质折叠，并被认为有助于细胞存活。使用大鼠C6胶质瘤细胞系和流式细胞术，我们评估了GRP 78表达后衣霉素和谷氨酸诱导的ER应激。结果表明，GRP 78表达上调后ER应激和损伤的胶质细胞具有保护作用。Annexin V和碘化丙啶标记显示，在损伤前瞬时表达GRP 78的细胞在72 h内受到高浓度衣霉素和谷氨酸的保护。我们的研究结果支持GRP 78抑制与ER应激相关的细胞死亡的假设。(C)2011爱思唯尔爱尔兰有限公司保留所有权利。
Endoplasmic reticulum (ER) stress induces apoptotic cell death by causing the accumulation of structurally abnormal proteins. The 78-kDa glucose-regulated protein (GRP78) is an ER chaperone that regulates protein folding in the ER and has been suggested to contribute to cell survival. Using the rat C6 glioma cell line and flow cytometry, we assessed GRP78 expression following tunicamycin- and glutamate-induced ER stress. The results showed that GRP78 expression is upregulated following ER stress and has protective effects on injured glial cells. Annexin V and propidium iodide labeling revealed cells transiently expressing GRP78 prior to injury were protected against high-concentrations of tunicamycin and glutamate within 72 h. Our findings support the hypothesis that GRP78 inhibits cell death associated with ER stress. (C) 2011 Elsevier Ireland Ltd. All rights reserved.