Gschwentner M, Nagl U O, Wöll E, Schmarda A, Ritter M, Paulmichl M
Department of Physiology, University of Innsbruck, Austria.
Pflugers Arch. 1995 Aug;430(4):464-70. doi: 10.1007/BF00373882.
Cell volume regulation is an essential feature of most cells. After swelling in hypotonic media, the simultaneous activation of potassium and chloride channels is believed to be the initial, time-determining step in cell volume regulation. The activation of both pathways is functionally linked and enables the cells to lose ions and water, subsequently leading to cell shrinkage and readjustment of the initial volume. NIH 3T3 fibroblasts efficiently regulate their volume after swelling and bear chloride channels that are activated by decreasing extracellular osmolarity. The chloride current elicited in these cells after swelling is reminiscent of the current found in oocytes expressing an outwardly rectifying chloride current termed ICln. Introduction of antisense oligodeoxynucleotides complementary to the first 30 nucleotides of the coding region of the ICln channel into NIH 3T3 fibroblasts suppresses the activation of the swelling-induced chloride current. The experiments directly demonstrate an unambiguous link between a volume-activated chloride current and a cloned protein involved in chloride transport.
细胞体积调节是大多数细胞的一个基本特征。在低渗介质中肿胀后，钾通道和氯通道的同时激活被认为是细胞体积调节中最初的、决定时间的步骤。这两条途径的激活在功能上相互关联，使细胞能够丢失离子和水分，随后导致细胞收缩并重新调整初始体积。NIH 3T3成纤维细胞在肿胀后能有效地调节其体积，并带有因细胞外渗透压降低而被激活的氯通道。这些细胞在肿胀后引发的氯电流让人联想到在表达一种名为ICln的外向整流氯电流的卵母细胞中发现的电流。将与ICln通道编码区前30个核苷酸互补的反义寡脱氧核苷酸导入NIH 3T3成纤维细胞，可抑制肿胀诱导的氯电流的激活。这些实验直接证明了体积激活的氯电流与参与氯转运的一种克隆蛋白之间存在明确的联系。
