缺氧通过上调TMEM16A钙激活氯通道增加脑微血管内皮细胞的增殖。
Hypoxia increases the proliferation of brain capillary endothelial cells via upregulation of TMEM16A Ca-activated Cl channels.
作者信息
Suzuki Takahisa, Suzuki Yoshiaki, Asai Kiyofumi, Imaizumi Yuji, Yamamura Hisao
机构信息
Department of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabedori Mizuhoku, Nagoya 467-8603, Japan.
Department of Molecular Neurobiology, Graduate School of Medical Sciences, Nagoya City University, 1 Kawasumi Mizuhocho Mizuhoku, Nagoya 467-8601, Japan.
出版信息
J Pharmacol Sci. 2021 May;146(1):65-69. doi: 10.1016/j.jphs.2021.03.002. Epub 2021 Mar 15.
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 Ca-activated Cl (Cl) channels, TMEM16A, were examined in bovine brain endothelial t-BBEC117 cells and mouse BCECs. The expression of TMEM16A was upregulated by hypoxia. Whole-cell Cl currents increased under hypoxia. Hypoxia also increased cell proliferation and trans-endothelial permeability, which were attenuated by Cl channel blockers or TMEM16A siRNA. These findings are useful for elucidating the pathological role of TMEM16A Cl channels in the BBB during cerebral ischemia.
血脑屏障（BBB）主要由脑毛细血管内皮细胞（BCECs）形成，在病理条件下会暴露于缺氧环境中。在牛脑内皮t-BBEC117细胞和小鼠BCECs中研究了缺氧对钙激活氯（Cl）通道TMEM16A表达和活性的影响。缺氧使TMEM16A的表达上调。缺氧条件下全细胞Cl电流增加。缺氧还增加了细胞增殖和跨内皮通透性，而Cl通道阻滞剂或TMEM16A siRNA可减弱这些作用。这些发现有助于阐明脑缺血期间TMEM16A Cl通道在血脑屏障中的病理作用。
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