The regulation of membrane 125I‐ and 86Rb+ permeability in a virally transformed cell line (NCL‐SG3) derived from the human sweat gland epithelium
The regulation of membrane 125I‐ and 86Rb+ permeability in a virally transformed cell line (NCL‐SG3) derived from the human sweat gland epithelium
复制标题
源自人汗腺上皮的病毒转化细胞系 (NCL-SG3) 膜 125I- 和 86Rb+ 通透性的调节
作者：
S. Wilson;M. Whiteford;D. Bovell;J. Pediani;W. Ko;Godfrey L. Smith;C. M. Lee;H. Y. Elder
我们已经探索了可能调节人汗腺上皮细胞系（NCL-SG 3）中膜通透性的因素。离子霉素增加了125 I-从预载细胞中流出的速率，这一作用似乎是由于细胞内游离钙（[Ca 2 +]i）增加。在存在高浓度外部钾的情况下，在暴露于钡或缬氨霉素的细胞中，离子霉素诱发的125 I外排增加减少。因此，离子霉素引起的125 I-流出增加的一部分是由于钾通道的激活，使用86 Rb+的实验也表明离子霉素增加了钾流出的速率，钡完全消除了这种作用。阻断Na（+）-K（+）-2Cl-共转运和Cl--HCO 3-交换降低了对照细胞和缬氨霉素去极化细胞125 I-外排的基础速率和离子霉素诱发的125 I-外排增加。因此，这些转运系统有助于阴离子流出，尽管[Ca 2 +]i依赖性氯离子通道似乎也存在。乙酰胆碱增加人汗腺分泌细胞中的[Ca 2 +]i，但这种神经递质不增加NCL-SG 3细胞中的[Ca 2 +]i，因此膜通透性不受胆碱能控制。肾上腺素不增加[Ca 2 +]i，但这种激素确实引起环磷酸腺苷（cAMP）的产生。然而，膜通透性不受肾上腺素能控制，因为细胞似乎不表达功能性环AMP依赖性阴离子通道。这可能是因为它们在培养条件下没有完全分化。ATP持续诱发阴离子外排的剂量依赖性增加，似乎由[Ca 2 +]i介导。[Ca 2 +]i的增加是由钙从有限的内部储存中释放引起的，随后由钙内流维持。UTP和ADP也增加[Ca 2 +]i，而腺苷、AMP和α，β-亚甲基ATP则无影响。因此，这些数据表明，在这些细胞中存在2型嘌呤受体的一个亚类，其在功能上与磷酸肌醇酶C偶联。
We have explored the factors that may regulate membrane permeability in a cell line (NCL‐SG3) derived from the human sweat gland epithelium. Ionomycin increased the rate of 125I‐efflux from preloaded cells and this action appeared to be due to an increase in intracellular free calcium ([Ca2+]i). The ionomycin‐evoked increase in 125I‐ efflux was reduced in cells that were exposed either to barium or to valinomycin in the presence of a high concentration of external potassium. It thus appears that a fraction of the ionomycin‐evoked increase in 125I‐ efflux is due to the activation of potassium channels and experiments using 86Rb+ also suggested that ionomycin increased the rate of potassium efflux, an effect which was totally abolished by barium. Blockade of Na(+)‐K(+)‐2Cl‐ cotransport and of Cl‐ ‐HCO3‐ exchange reduced the basal rate of 125I‐ efflux and the ionomycin‐evoked increase in 125I‐efflux from control cells and from cells depolarized by valinomycin. These transport systems thus contribute to anion efflux, although [Ca2+]i‐dependent chloride channels also appear to be present. Acetylcholine increases [Ca2+]i in the secretory cells of human sweat glands, but this neurotransmitter did not increase [Ca2+]i in NCL‐SG3 cells and so membrane permeability was not under cholinergic control. Adrenaline did not increase [Ca2+]i, but this hormone did evoke cyclic‐3',5'‐adenosine monophosphate (cyclic AMP) production. However, membrane permeability was not under adrenergic control, as the cells did not appear to express functional, cyclic AMP‐dependent anion channels. This may be because they were not fully differentiated under the culture conditions. ATP consistently evoked a dose‐dependent increase in anion efflux that appeared to be mediated by [Ca2+]i. The increase in [Ca2+]i was initiated by the release of calcium from a limited internal store and was subsequently sustained by calcium influx. UTP and ADP also increased [Ca2+]i, whereas adenosine, AMP and alpha,beta‐methylene ATP were without effect. These data thus suggest that a subclass of type 2 purine receptor, which is functionally coupled to phosphoinositidase C, is present in these cells.