Chloride channel regulation in secretory epithelia.
Chloride channel regulation in secretory epithelia.
复制标题
DOI：
--
复制
发表时间：
1986-11
期刊：
影响因子：
--
通讯作者：
R. Frizzell;D. Halm;G. Rechkemmer;R. Shoemaker
中科院分区：
文献类型：
--
作者：
R. Frizzell;D. Halm;G. Rechkemmer;R. Shoemaker
应用膜片钳技术对氯离子分泌上皮细胞、人气道上皮细胞和T84细胞进行单通道记录。肾上腺素或环磷酸腺苷(CAMP)在细胞附着记录过程中刺激人呼吸道细胞的单通道活动。同样，前列腺素E2和cAMP刺激T84细胞的单通道活动。离子置换实验表明，在两种细胞类型的通道中，氯与钠的选择性大于10：1，这证实了这些事件是氯通道的开放。钙离子载体A23187刺激这两种类型的细胞开放这些氯离子通道。囊性纤维化(CF)患者的人呼吸道细胞对肾上腺素或cAMP无反应，但A23187处理可引起氯通道活动。由内向外构型的浴液钙活性的变化表明，钙的增加可以激活CF细胞上cAMP不敏感的氯通道。这表明，Cf的主要缺陷在于对氯通道开放的调节，而不是氯通过通道的传导。
Patch-clamp techniques were applied for single-channel recording to cultured cells from Cl secretory epithelia: human airway cells and the T84 cell line. Epinephrine or cyclic AMP (cAMP) stimulated single-channel activity in human airway cells during cell-attached recording. Similarly, prostaglandin E2 and cAMP stimulated single-channel activity in T84 cells. Ion substitution experiments with patches in the inside-out configuration indicated greater than 10:1 selectivity for Cl over Na in channels from both cell types, which confirms the identity of these events as Cl channel openings. The Ca ionophore A23187 stimulated these Cl channels to open in both cell types. Human airway cells from patients with cystic fibrosis (CF) did not respond to epinephrine or cAMP, but A23187 treatment elicited Cl channel activity. Changes in bath Ca activity in the inside-out configuration demonstrated that increased Ca could activate cAMP-insensitive Cl channels in CF cells. This indicates that the primary defect in CF is in the regulation of Cl channel opening rather than in conduction of Cl through the channel.