title: Membrane hyperpolarization induced by endoplasmic reticulum stress facilitates ca(2+) influx to regulate cell cycle progression in brain capillary endothelial cells.
abstract: 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 Ca(2+) concentration ([Ca(2+)]i) and a facilitation of cell death. Expressions of Ca(2+) influx channels (TRPC, Orai1, STIM1) were unchanged by ER stress. The ER stress-induced [Ca(2+)]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.
authors.affiliation: Department of Molecular & Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Kito
authors.forename: Hisao
authors.initials: H
authors.lastname: Yamamura
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Susumu
authors.initials: S
authors.lastname: Ohya
authors.forename: Kiyofumi
authors.initials: K
authors.lastname: Asai
authors.forename: Yuji
authors.initials: Y
authors.lastname: Imaizumi
mesh_terms: D000818:Animals; D001921:Brain / Q000166:cytology*; D002118:Calcium / Q000378:metabolism*; D002417:Cattle; D002453:Cell Cycle / Q000502:physiology*; D016923:Cell Death; D002460:Cell Line; D059865:Endoplasmic Reticulum Stress / Q000502:physiology*; D042783:Endothelial Cells / Q000166:cytology*; D008564:Membrane Potentials / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*
chemical_list: C489461:Kir2.1 channel; D024661:Potassium Channels, Inwardly Rectifying; D002118:Calcium