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首页> 外文期刊>American Journal of Physiology >Osmotic swelling-provoked release of organic osmolytes in human intestinal epithelial cells.
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Osmotic swelling-provoked release of organic osmolytes in human intestinal epithelial cells.

机译：渗透溶胀引起的有机渗透物在人肠上皮细胞中的释放。

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Human Intestine 407 cells respond to osmotic cell swelling by the activation of Cl(-)- and K(+)-selective ionic channels, as well as by stimulating an organic osmolyte release pathway readily permeable to taurine and phosphocholine. Unlike the activation of volume-regulated anion channels (VRAC), activation of the organic osmolyte release pathway shows a lag time of approximately 30-60 s, and its activity persists for at least 8-12 min. In contrast to VRAC activation, stimulation of organic osmolyte release did not require protein tyrosine phosphorylation, active p21(rho), or phosphatidylinositol 3-kinase activity and was insensitive to Cl(-) channel blockers. Treatment of the cells with putative organic anion transporter inhibitors reduced the release of taurine only partially or was found to be ineffective. The efflux was blocked by a subclass of organic cation transporter (OCT) inhibitors (cyanine-863 and decynium-22) but not by other OCT inhibitors (cimetidine, quinine, and verapamil). Brief treatment of the cells with phorbol esters potentiated the cell swelling-induced taurine efflux, whereas addition of the protein kinase C (PKC) inhibitor GF109203X largely inhibited the response, suggesting that PKC is involved. Increasing the level of intracellular Ca(2+) by using A-23187- or Ca(2+)-mobilizing hormones, however, did not affect the magnitude of the response. Taken together, the results indicate that the hypotonicity-induced efflux of organic osmolytes is independent of VRAC and involves a PKC-dependent step.
机译：人肠407细胞通过激活Cl（-）和K（+）选择性离子通道，以及刺激牛磺酸和磷酸胆碱易于渗透的有机渗透液释放途径，对渗透细胞肿胀作出反应。与体积调节阴离子通道（VRAC）的激活不同，有机渗透液释放途径的激活显示约30-60 s的滞后时间，并且其活性持续至少8-12分钟。与VRAC激活相反，有机渗透压释放的刺激不需要蛋白质酪氨酸磷酸化，活性p21（rho）或磷脂酰肌醇3激酶活性，并且对Cl（-）通道阻滞剂不敏感。用推定的有机阴离子转运蛋白抑制剂处理细胞只能部分或部分降低牛磺酸的释放或发现无效。外排被一类有机阳离子转运蛋白（OCT）抑制剂（花菁863和十cy-22）阻止，但未被其他OCT抑制剂（西咪替丁，奎宁和维拉帕米）阻止。用佛波酯短暂处理细胞可增强细胞膨胀诱导的牛磺酸外排，而添加蛋白激酶C（PKC）抑制剂GF109203X则在很大程度上抑制了这种反应，表明参与了PKC。通过使用A-23187-或Ca（2+）动员激素来增加细胞内Ca（2+）的水平，但不影响响应的程度。两者合计，结果表明低渗诱导的有机渗透物外排独立于VRAC，并涉及PKC依赖的步骤。

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