IK channels are involved in the regulatory volume decrease in human epithelial cells.
IK channels are involved in the regulatory volume decrease in human epithelial cells.
复制标题
DOI：
10.1152/ajpcell.00132.2002
复制
发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Jun Wang;S. Morishima;Y. Okada
中科院分区：
文献类型：
--
作者：
Jun Wang;S. Morishima;Y. Okada
已知 Ca(2+) 依赖性 K(+) 通道和体积敏感 Cl(-) 通道的并行激活是人上皮肠 407 细胞调节体积减少 (RVD) 期间 KCl 流出的原因。本研究的目的是确定 K(+) 通道类型。 RT-PCR 证明该细胞系中 Ca(2+) 激活的中等电导 K(+) (IK) 通道的 mRNA 表达，但不表达小电导 K(+) (SK1) 或大电导 K(+) (BK) 通道。全细胞记录显示，离子霉素或低渗应激激活内向整流 K(+) 电流，该电流可被 IK 通道阻滞剂 [克霉唑 (CLT) 和 Charybdotoxin] 可逆性阻断，但不会被 SK 和 BK 通道阻滞剂（apamin 和 iberiotoxin）阻断。由内而外的记录揭示了 CLT 敏感的单 K(+) 通道活动的存在，该活动表现出中间单一电导（-100 mV 时为 30 pS）。该通道由内向外斑块中的胞质 Ca(2+) 和细胞附着斑块中的低渗激发激活。 RVD 被 CLT 抑制，但不能被 apamin 或伊比利亚毒素抑制。因此我们得出结论，IK 通道参与了这些人类上皮细胞的 RVD 过程。
Parallel activation of Ca(2+)-dependent K(+) channels and volume-sensitive Cl(-) channels is known to be responsible for KCl efflux during regulatory volume decrease (RVD) in human epithelial Intestine 407 cells. The present study was performed to identify the K(+) channel type. RT-PCR demonstrated mRNA expression of Ca(2+)-activated, intermediate conductance K(+) (IK), but not small conductance K(+) (SK1) or large conductance K(+) (BK) channels in this cell line. Whole cell recordings showed that ionomycin or hypotonic stress activated inwardly rectifying K(+) currents that were reversibly blocked by IK channel blockers [clotrimazole (CLT) and charybdotoxin] but not by SK and BK channel blockers (apamin and iberiotoxin). Inside-out recordings revealed the existence of CLT-sensitive single K(+)-channel activity, which exhibited an intermediate unitary conductance (30 pS at -100 mV). The channel was activated by cytosolic Ca(2+) in inside-out patches and by a hypotonic challenge in cell-attached patches. The RVD was suppressed by CLT, but not by apamin or iberiotoxin. Thus we conclude that the IK channel is involved in the RVD process in these human epithelial cells.