Membrane Hyperpolarization Induced by Endoplasmic Reticulum Stress Facilitates Ca2+ Influx to Regulate Cell Cycle Progression in Brain Capillary Endothelial Cells

Journal of Pharmacological Sciences

Susumu Ohya¹  Yuji Imaizumi²  Hisao Yamamura²  Hiroaki Kito²  Yoshiaki Suzuki²  Kiyofumi Asai³ 

[1] Department of Pharmacology, Division of Pathological Sciences, Kyoto Pharmaceutical University, Japan;Department of Molecular & Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Japan;Department of Molecular Neurobiology, Graduate School of Medical Sciences, Nagoya City University, Japan

关键词: brain capillary endothelial cell;    store operated calcium entry;    endoplasmic reticulum stress;   

DOI  :  10.1254/jphs.14002SC

学科分类：药学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(15)Cited-By(3)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, Orai1, 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.

【 授权许可】

Unknown