| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10763109 | Biochemical and Biophysical Research Communications | 2011 | 6 Pages |
Abstract
⺠We found that application of endoplasmic reticulum (ER) stress with tunicamycin to brain capillary endothelial cells (BCECs) induced cell death. ⺠The ER stress facilitated the expression of inward rectifier K+ channel (Kir2.1) and induced sustained membrane hyperpolarization. ⺠The membrane hyperpolarization induced sustained Ca2+ entry through voltage-independent nonspecific cation channels and consequently facilitated cell death. ⺠The Kir2.1 up-regulation by ER stress is, at least in part, responsible for cell death of BCECs under pathological conditions.
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Authors
Hiroaki Kito, Daiju Yamazaki, Susumu Ohya, Hisao Yamamura, Kiyofumi Asai, Yuji Imaizumi,