GRP94 reduces cell death in SH-SY5Y cells perturbated calcium homeostasis
GRP94 reduces cell death in SH-SY5Y cells perturbated calcium homeostasis
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DOI：
10.1023/b:appt.0000031446.95532.ad
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发表时间：
2004-07-01
期刊：
影响因子：
7.2
通讯作者：
Tohyama, M
中科院分区：
文献类型：
--
作者：
Bando, Y;Katayama, T;Tohyama, M
内质网（ER）驻留-94 kDa葡萄糖调节蛋白（GRP 94），在由于ER应激引起的细胞死亡中起关键作用。在我们的研究中，由于暴露于钙离子载体A23187，GRP 94在人神经母细胞瘤SH-SY 5 Y细胞中的表达增加。A23187介导的细胞死亡与主要半胱氨酸蛋白酶caspase-3和钙蛋白酶的激活有关。与野生型细胞或腺病毒介导的GRP 94过表达的细胞（AdGRP 94 S）相比，腺病毒介导的反义GRP 94（AdGRP 94 AS）预处理降低了经受A23187处理的SH-SY 5 Y细胞的存活率。这些结果表明GRP 94的抑制与加速的细胞死亡有关。此外，GRP 94的表达抑制A23187诱导的细胞死亡和稳定的钙稳态。
The endoplasmic reticulum (ER) resident-94 kDa glucose-regulated protein (GRP94), plays a pivotal role in cell death due to ER stress. In our study expression of GRP94 was increased in human neuroblastoma SH-SY5Y cells due to exposure to calcium ionophore A23187. A23187-mediated cell death was associated with activation of the major cysteine proteases, caspase-3 and calpain. Pretreatment with adenovirus-mediated antisense GRP94 (AdGRP94AS) reduced viability of SH-SY5Y cells subjected to A23187 treatment compared with wild type cells or cells with adenovirus-mediated overexpression of GRP94 (AdGRP94S). These results indicated that suppression of GRP94 is associated with accelerated cell death. Moreover, expression of GRP94 suppressed A23187-induced cell death and stabilized calcium homeostasis.