Membrane Hyperpolarization Induced by Endoplasmic Reticulum Stress Facilitates Ca2+ Influx to Regulate Cell Cycle Progression in Brain Capillary Endothelial Cells
Membrane Hyperpolarization Induced by Endoplasmic Reticulum Stress Facilitates Ca2+ Influx to Regulate Cell Cycle Progression in Brain Capillary Endothelial Cells
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DOI：
10.1254/jphs.14002sc
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发表时间：
2014-06-01
影响因子：
3.5
通讯作者：
Imaizumi, Yuji
中科院分区：
文献类型：
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作者：
Kito, Hiroaki;Yamamura, Hisao;Imaizumi, Yuji
Kir2.1通道在内质网（ER）应激过程中的上调在t-BBEC 117（一种永生化的牛脑内皮细胞系）中引起细胞内Ca 2+浓度（[Ca 2 +]i）的持续增加和促进细胞死亡。钙内流通道（TRPC、Orail、STIM 1）的表达不受ER应激的影响。ER应激诱导的[Ca 2 +]i增加主要归因于Kir2.1上调引起的更深的静息膜电位。ER应激在G2/M期被阻滞，并且它被Kir2.1的抑制剂减弱。这些结果表明，通过ER应激上调Kir2.1通过调节t-BBEC 117中的细胞周期进程促进细胞死亡。
Upregulation of the Kir2.1 channel during endoplasmic reticulum (ER) stress in t-BBEC117, an immortalized bovine brain endothelial cell line, caused a sustained increase in intracellular Ca2+ concentration ([Ca2+]i) and a facilitation of cell death. Expressions of Ca2+ influx channels (TRPC, Orail, STIM1) were unchanged by ER stress. The ER stress-induced [Ca2+]i increase was mainly attributed to the deeper resting membrane potential due to Kir2.1 upregulation. ER stress arrested at the G2/M phase and it was attenuated by an inhibitor of Kir2.1. These results indicate that Kir2.1 upregulation by ER stress facilitates cell death via regulation of cell cycle progression in t-BBEC117.