Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca2+-activated Cl- channels.
Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca2+-activated Cl- channels.
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DOI：
10.1016/j.jphs.2021.03.002
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发表时间：
2021-05
影响因子：
3.5
通讯作者：
Takahisa Suzuki;Yoshiaki Suzuki;K. Asai;Y. Imaizumi;H. Yamamura
中科院分区：
文献类型：
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作者：
Takahisa Suzuki;Yoshiaki Suzuki;K. Asai;Y. Imaizumi;H. Yamamura
血脑屏障（BBB）主要由脑毛细血管内皮细胞（BCECs）形成，在病理条件下暴露于缺氧环境。在牛脑内皮t-BBEC 117细胞和小鼠BCECs中检测了缺氧对Ca 2+激活的Cl−（ClCa）通道TMEM 16 A的表达和活性的影响。缺氧可上调TMEM 16 A的表达。缺氧时全细胞ClCacurrent增加。缺氧还增加细胞增殖和跨内皮渗透性，这被ClCachanel阻断剂或TMEM 16 A siRNA减弱。这些发现有助于阐明脑缺血时TMEM 16 AClCa通道在血脑屏障中的病理作用。
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 ClCacurrents increased under hypoxia. Hypoxia also increased cell proliferation and trans-endothelial permeability, which were attenuated by ClCachannel blockers or TMEM16A siRNA. These findings are useful for elucidating the pathological role of TMEM16A ClCachannels in the BBB during cerebral ischemia.