Cl⁻ channels in smooth muscle cells.
Cl⁻ channels in smooth muscle cells.
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DOI：
10.1007/s00424-013-1357-2
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发表时间：
2014-05
影响因子：
4.5
通讯作者：
Jaggar, Jonathan H.
中科院分区：
文献类型：
--
作者：
Bulley, Simon;Jaggar, Jonathan H.
在平滑肌细胞（SMC）中，由于Cl−/HCO 3 −交换和Na+、K+、Cl−共转运的积累，细胞内Cl−浓度很高。Cl−的平衡电位（ECl）比生理膜电位（Em）更正，Cl−流出诱导膜去极化。早期的研究使用电生理学和非特异性拮抗剂来研究SMC中Cl−通道的生理相关性。最近的报告已经结合分子生物学方法来识别和确定几种不同的Cl−通道的功能意义。“经典”和cGMP依赖性钙（Ca 2+）激活（ClCa）通道和体积敏感性Cl−通道都存在，TMEM 16 A/ANO 1、雌激素和ClC-3分别被认为是这些通道的分子候选者。囊性纤维化跨膜传导调节因子（CFTR）也已在SMC中描述。本文将重点讨论最近在确定这些Cl−通道在SMCs，其生理功能，并修改收缩，凋亡和细胞增殖的疾病的贡献取得的进展。
In smooth muscle cells (SMCs), the intracellular chloride ion (Cl−) concentration is high due to accumulation by Cl−/HCO3− exchange and Na+, K+, Cl− cotransportation. The equilibrium potential for Cl− (ECl) is more positive than physiological membrane potentials (Em), with Cl− efflux inducing membrane depolarization. Early studies used electrophysiology and non-specific antagonists to study the physiological relevance of Cl− channels in SMCs. More recent reports have incorporated molecular biological approaches to identify and determine the functional significance of several different Cl− channels. Both “classic” and cGMP-dependent calcium (Ca2+)-activated (ClCa) channels and volume-sensitive Cl− channels are present, with TMEM16A/ANO1, bestrophins and ClC-3, respectively, proposed as molecular candidates for these channels. The cystic fibrosis transmembrane conductance regulator (CFTR) has also been described in SMCs. This review will focus on discussing recent progress made in identifying each of these Cl− channels in SMCs, their physiological functions, and contribution to diseases that modify contraction, apoptosis and cell proliferation.
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DOI：
10.1085/jgp.200609581
发表时间：
2006-09
期刊：
The Journal of general physiology
影响因子：
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作者：
Chien LT;Zhang ZR;Hartzell HC
通讯作者：
Hartzell HC
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影响因子：
5.5
作者：
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通讯作者：
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DOI：
10.1152/ajpheart.2001.281.5.h2159
发表时间：
2001-11-01
影响因子：
4.8
作者：
Dai, Y;Zhang, JH
通讯作者：
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影响因子：
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作者：
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DOI：
10.1152/ajpcell.1998.275.4.c940
发表时间：
1998-10-01
影响因子：
5.5
作者：
Dick, GM;Bradley, EK;Sanders, KM
通讯作者：
Sanders, KM