An increase in intracellular Cl- concentration ([Cl-]i) may be a general response of airway epithelial cells to various stimuli and may participate in some basic cellular functions. However, whether the basic functional activities of cells, such as proliferation and wound healing, are related to Cl- activities remains unclear. This study aimed to investigate the effects and potential mechanisms of [Cl-]i on the proliferation and wound healing ability of airway epithelial BEAS-2B cells. BEAS-2B cells were treated with four Cl- channel inhibitors (T16Ainh-A01, CFTRinh-172, CaCCinh-A01, and IAA-94), and the Cl- fluorescence probe N-(ethoxycarbonylmethyl)-6-methoxyquinolinium bromide was used. Results showed that all Cl- channel inhibitors could increase [Cl-]i in BEAS-2B cells. The increased [Cl-]i induced by Cl- channel inhibitors or clamping [Cl-]i at high levels enhanced the phosphorylation of focal adhesion kinase (FAK) and subsequently promoted the proliferation and wound healing ability of BEAS-2B cells. By contrast, the FAK inhibitor PF573228 abrogated these effects induced by the increased [Cl-]i. FAK also activated the PI3K/AKT signaling pathway. In conclusion, increased [Cl-]i promotes the proliferation and wound healing ability of BEAS-2B cells by activating FAK to activate the PI3K/AKT signaling pathway. Intracellular Cl- may act as a signaling molecule to regulate the proliferation and wound healing ability of airway epithelial cells.

中文翻译：

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通过激活FAK增加的细胞内Cl浓度可促进气道上皮BEAS-2B细胞增殖和伤口愈合。

细胞内Cl-浓度（[Cl-] i）的增加可能是气道上皮细胞对各种刺激的普遍反应，并且可能参与一些基本的细胞功能。但是，尚不清楚细胞的基本功能活性（例如增殖和伤口愈合）是否与Cl-活性有关。本研究旨在探讨[Cl-] i对气道上皮BEAS-2B细胞增殖和伤口愈合能力的影响及其潜在机制。用四种Cl通道抑制剂（T16Ainh-A01，CFTRinh-172，CaCCinh-A01和IAA-94）处理BEAS-2B细胞，并使用Cl-荧光探针N-（乙氧羰基甲基）-6-甲氧基喹啉溴化物。结果表明，所有Cl通道抑制剂均可增加BEAS-2B细胞中的[Cl-] i。Cl-通道抑制剂诱导的[Cl-] i升高或高水平钳制[Cl-] i增强了粘着斑激酶（FAK）的磷酸化，随后促进了BEAS-2B细胞的增殖和伤口愈合能力。相比之下，FAK抑制剂PF573228消除了由[Cl-] i升高引起的这些作用。FAK还激活了PI3K / AKT信号通路。总之，增加的[Cl-] i通过激活FAK激活PI3K / AKT信号通路来促进BEAS-2B细胞的增殖和伤口愈合能力。细胞内Cl-可以作为信号分子来调节气道上皮细胞的增殖和伤口愈合能力。FAK抑制剂PF573228消除了由[Cl-] i升高引起的这些作用。FAK还激活了PI3K / AKT信号通路。总之，增加的[Cl-] i通过激活FAK激活PI3K / AKT信号通路来促进BEAS-2B细胞的增殖和伤口愈合能力。细胞内Cl-可以作为信号分子来调节气道上皮细胞的增殖和伤口愈合能力。FAK抑制剂PF573228消除了由[Cl-] i升高引起的这些作用。FAK还激活了PI3K / AKT信号通路。总之，增加的[Cl-] i通过激活FAK激活PI3K / AKT信号通路来促进BEAS-2B细胞的增殖和伤口愈合能力。细胞内Cl-可以作为信号分子来调节气道上皮细胞的增殖和伤口愈合能力。