Referenced in: none

Automatically associated channels: Kir2.1 , TRP , TRPC

Title: Membrane hyperpolarization induced by endoplasmic reticulum stress facilitates ca(2+) influx to regulate cell cycle progression in brain capillary endothelial cells.

Authors: Hiroaki Kito, Hisao Yamamura, Yoshiaki Suzuki, Susumu Ohya, Kiyofumi Asai, Yuji Imaizumi

Journal, date & volume: J. Pharmacol. Sci., 2014 , 125, 227-32

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/24859777

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.