Intermediate-conductance calcium-activated potassium channel KCa3.1 and chloride channel modulate chemokine ligand (CCL19/CCL21)-induced migration of dendritic cells.
Intermediate-conductance calcium-activated potassium channel KCa3.1 and chloride channel modulate chemokine ligand (CCL19/CCL21)-induced migration of dendritic cells.
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DOI：
10.1016/j.trsl.2014.11.010
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发表时间：
2015-07
期刊：
影响因子：
--
通讯作者：
Agrawal DK
中科院分区：
文献类型：
--
作者：
Shao Z;Gaurav R;Agrawal DK
离子通道在趋化因子诱导的非兴奋细胞如树突状细胞迁移中的作用在很大程度上是未知的。在这里，我们研究了KCa3.1和氯离子通道在淋巴趋化因子诱导的树突状细胞迁移中的作用。CCL 19/21诱导的Ca 2+内流的幅度和动力学与CCR 7表达水平、细胞外游离Ca 2+和Cl−相关，而与细胞外K+无关。趋化因子CCL 19和CCL 21以及KCa3.1激活剂1-EBIO诱导质膜超极化和K+流出，这被TRAM-34阻断，表明KCa3.1比内向CRAC具有更大的电导。阻断KCa3.1、培养基中的低Cl−和低剂量的DIDS损害了CCL 19/CCL 21诱导的Ca 2+内流、细胞体积变化和DC迁移。高剂量的DIDS可能通过显著破坏线粒体膜电位而完全阻断DC迁移。总之，KCa3.1和氯离子通道通过协同调节膜电位、趋化因子诱导的Ca 2+内流和细胞体积在人DC迁移中至关重要。
The role of ion channels is largely unknown in chemokine-induced migration in non-excitable cells such as dendritic cells. Here, we examined the role of KCa3.1 and chloride channels in lymphatic chemokines-induced migration of dendritic cells. The amplitude and kinetics of CCL19/21-induced Ca2+ influx were associated with CCR7 expression levels, extracellular free Ca2+ and Cl−, and independent of extracellular K+. Chemokines, CCL19 and CCL21, and KCa3.1 activator, 1-EBIO, induced plasma membrane hyperpolarization and K+ efflux, which was blocked by TRAM-34, suggesting that KCa3.1 carried larger conductance than the inward CRAC. Blockade of KCa3.1, low Cl− in the medium, and low dose of DIDS impaired CCL19/CCL21-induced Ca2+ influx, cell volume change, and DC migration. High doses of DIDS completely blocked DC migration possibly by significantly disrupting mitochondrial membrane potential. In conclusion, KCa3.1 and chloride channel are critical in human DC migration by synergistically regulating membrane potential, chemokine-induced Ca2+ influx, and cell volume.
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影响因子：
5.4
作者：
Duffy, S. Mark;Cruse, Glenn;Cockerill, Sarah L.;Brightling, Chris E.;Bradding, Peter
通讯作者：
Bradding, Peter
影响因子：
8.7
作者：
通讯作者：
--
DOI：
10.1085/jgp.20028551
发表时间：
2002-05
期刊：
The Journal of general physiology
影响因子：
--
作者：
Prakriya M;Lewis RS
通讯作者：
Lewis RS
影响因子：
64.8
作者：
Graves, Austin R.;Curran, Patricia K.;Mindell, Joseph A.
通讯作者：
Mindell, Joseph A.
影响因子：
4.4
作者：
Gaurav R;Agrawal DK
通讯作者：
Agrawal DK