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作 者:何伟[1] 李辉[1] 刘杰[2] 史路平[2] 张知非[2] 徐萌[2] 王军[2]
机构地区:[1]首都医科大学附属北京朝阳医院胸外科,100020 [2]首都医科大学基础医学院
出 处:《中华医学杂志》2009年第45期3220-3223,共4页National Medical Journal of China
基 金:国家自然科学基金(30670765);北京市教育委员会科技发展计划(KM200710025019)
摘 要:目的观察人肺腺癌细胞调节性细胞容积减小(RVD)的过程,探讨其离子通道机制。方法用细胞体积测量系统分析人肺腺癌细胞(A549)在细胞外低渗刺激下细胞容积改变;用通道阻断剂和全细胞膜片钳方法阐明容积敏感性氯通道在RVD中的作用。结果细胞外低渗刺激使人肺腺癌细胞系A549细胞膨胀并诱发RVD,该RVD过程可被氯通道阻断剂NPPB(100μmo//L)和钾通道阻断剂CsCl(5mmol/L)所阻抑;全细胞膜片钳方法记录A549细胞容积敏感性氯通道电流呈外向整流特性,电流可被NPPB、DIDS(100μmol/L)阻抑。结论人肺腺癌A549细胞具有RVD功能,RVD过程的完成有赖于氯通道和钾通道的平行激活,容积敏感性氯通道参与该RVD过程。Objective This study was designed to observe the regulatory volume decrease (RVD) process in human lung adenocarcinoma cells (A549) and to investigate its ion channel mechanism. Methods Electric measurement system of cell volume was used to detect the cell volume changes following exposure to hypotonic solution. Whole-cell patch clamp recordings were applied to investigate the characteristics of the volume-sensitive Cl^- channel in A549 cells. Results Extracelluar hypotonicity induced cell swelling followed by a typical RVD process, which can be inhibited by Cl^- channel blocker ( NPPB 100 μmoVL) and K^+ channel blocker ( CsCl 5 mmol/L). Meanwhile, a outward-rectifying chloride currents which was sensitive to NPPB and DIDs was recorded in A549 using the whole cell patch clamp. Conclusions The human lung adenocarcinoma cells has RVD process which is dependent on the parallel activation of Cl^- channel and K^+ channel. The volume-sensitive Cl^- channel is involved in volume regulation of lung adenocarcinoma cells.
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