Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca2+-activated Cl− channels
The blood–brain barrier (BBB) is mainly formed by brain capillary endothelial cells (BCECs) and is exposed to hypoxic environments under pathological conditions. The effects of hypoxia on the expression and activity of Ca2+-activated Cl− (ClCa) channels, TMEM16A, were examined in bovine brain endoth...
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doaj-4968c6615d40456fad391e34b64d3d942021-04-14T04:15:09ZengElsevierJournal of Pharmacological Sciences1347-86132021-05-0114616569Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca2+-activated Cl− channelsTakahisa Suzuki0Yoshiaki Suzuki1Kiyofumi Asai2Yuji Imaizumi3Hisao Yamamura4Department of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabedori Mizuhoku, Nagoya 467-8603, JapanDepartment of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabedori Mizuhoku, Nagoya 467-8603, JapanDepartment of Molecular Neurobiology, Graduate School of Medical Sciences, Nagoya City University, 1 Kawasumi Mizuhocho Mizuhoku, Nagoya 467-8601, JapanDepartment of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabedori Mizuhoku, Nagoya 467-8603, JapanDepartment of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabedori Mizuhoku, Nagoya 467-8603, Japan; Corresponding author. Fax: +81 52 836 3431.The blood–brain barrier (BBB) is mainly formed by brain capillary endothelial cells (BCECs) and is exposed to hypoxic environments under pathological conditions. The effects of hypoxia on the expression and activity of Ca2+-activated Cl− (ClCa) channels, TMEM16A, were examined in bovine brain endothelial t-BBEC117 cells and mouse BCECs. The expression of TMEM16A was upregulated by hypoxia. Whole-cell ClCa currents increased under hypoxia. Hypoxia also increased cell proliferation and trans-endothelial permeability, which were attenuated by ClCa channel blockers or TMEM16A siRNA. These findings are useful for elucidating the pathological role of TMEM16A ClCa channels in the BBB during cerebral ischemia.http://www.sciencedirect.com/science/article/pii/S1347861321000220Brain capillary endothelial cellHypoxiaTMEM16A |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Takahisa Suzuki Yoshiaki Suzuki Kiyofumi Asai Yuji Imaizumi Hisao Yamamura |
spellingShingle |
Takahisa Suzuki Yoshiaki Suzuki Kiyofumi Asai Yuji Imaizumi Hisao Yamamura Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca2+-activated Cl− channels Journal of Pharmacological Sciences Brain capillary endothelial cell Hypoxia TMEM16A |
author_facet |
Takahisa Suzuki Yoshiaki Suzuki Kiyofumi Asai Yuji Imaizumi Hisao Yamamura |
author_sort |
Takahisa Suzuki |
title |
Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca2+-activated Cl− channels |
title_short |
Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca2+-activated Cl− channels |
title_full |
Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca2+-activated Cl− channels |
title_fullStr |
Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca2+-activated Cl− channels |
title_full_unstemmed |
Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca2+-activated Cl− channels |
title_sort |
hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of tmem16a ca2+-activated cl− channels |
publisher |
Elsevier |
series |
Journal of Pharmacological Sciences |
issn |
1347-8613 |
publishDate |
2021-05-01 |
description |
The blood–brain barrier (BBB) is mainly formed by brain capillary endothelial cells (BCECs) and is exposed to hypoxic environments under pathological conditions. The effects of hypoxia on the expression and activity of Ca2+-activated Cl− (ClCa) channels, TMEM16A, were examined in bovine brain endothelial t-BBEC117 cells and mouse BCECs. The expression of TMEM16A was upregulated by hypoxia. Whole-cell ClCa currents increased under hypoxia. Hypoxia also increased cell proliferation and trans-endothelial permeability, which were attenuated by ClCa channel blockers or TMEM16A siRNA. These findings are useful for elucidating the pathological role of TMEM16A ClCa channels in the BBB during cerebral ischemia. |
topic |
Brain capillary endothelial cell Hypoxia TMEM16A |
url |
http://www.sciencedirect.com/science/article/pii/S1347861321000220 |
work_keys_str_mv |
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