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首页> 外文期刊>Cell Research >Regulation of swelling-activated chloride channels in embryonic chick heart cells
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Regulation of swelling-activated chloride channels in embryonic chick heart cells

机译：胚胎鸡心脏细胞中溶胀激活的氯离子通道的调节

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摘要

Swelling-activated Cl~- currents, I_((Cl, swell)), were measured during hyposmotic shock in white Leghorn embryonic chick heart cells using the whole-cell recording of patch-clamp technique. Genistein, an inhibitor of protein tyrosine kinase (PTK), suppressed I_((Cl,swell)). Under isosmotic condition phorbol 12-myristate 13-acetate (PMA), an activator of PKC, elicited the Cl~- current similar to that in hyposmotic solution, whereas hyposmotic shock did not elicit I_((Cl,swell)) in chelerythrine chloride(an inhibitor of PKC)-treated cells. Con-focal microscopy experiments using FITC-phalloidin as a fluorescent label of F-actin showed that the actin network was moved from cortical region of the cell to the center after hyposmotic shock as compared with the image under isosmotic condition. When the cells were treated with cytochalasin B (CB) or cytochalasin D (CD) under isosmotic condition the disruption of the F-actin integrity was observed, and I_((Cl, swell)) was not elicited. With combination treatment of CB with PMA, hyposmotic solution could not elicited I_(Cl,swell)). The results suggested that the role of PTK, probably receptor tyrosine kinase, for regulation of I_((Cl,swell)) appeared to be at upstream site related to the role of F-actin. Then PKC signal pathway was activated somehow and finally change in the polymerization state of cytoskeleton led to activate the swelling-activated Cl~- channels. These results demonstrate clearly that PTK, PKC and F-actin are important factors for regulation of I_((Cl,swell)), in embryonic chick heart cells as compared with often controversial results reported in different cell types.
机译：使用膜片钳技术全细胞记录，在白色来格霍恩胚胎雏鸡心脏细胞低渗性休克期间测量了溶胀激活的Cl-电流I _（（Cl，swell））。 Genistein，蛋白酪氨酸激酶（PTK）的抑制剂，抑制了I _（（Cl，swell））。在等渗条件下，佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）是PKC的活化剂，其Cl-电流类似于低渗溶液中的Cl_-电流，而低渗休克不会引起白屈菜红素氯化物（ PKC处理细胞的抑制剂。使用FITC-鬼笔环肽作为F-肌动蛋白的荧光标记的共聚焦显微镜实验表明，与等渗条件下的图像相比，低渗性休克后肌动蛋白网络从细胞的皮质区域移动到中心。当在等渗条件下用细胞松弛素B（CB）或细胞松弛素D（CD）处理细胞时，观察到F-肌动蛋白完整性的破坏，并且未引起I _（（Cl，溶胀））。通过CB与PMA的联合处理，低渗溶液无法引发I_（Cl，swell））。结果表明，PTK（可能是受体酪氨酸激酶）对I _（（Cl，swell））的调节作用似乎在与F-肌动蛋白作用有关的上游位点。然后以某种方式激活了PKC信号通路，并最终改变了细胞骨架的聚合状态，从而激活了溶胀激活的Cl〜-通道。这些结果清楚地表明，与经常在不同细胞类型中报道的有争议的结果相比，在胚胎雏鸡心脏细胞中，PTK，PKC和F-肌动蛋白是调节I _（（Cl，swell））的重要因素。

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