• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Characterisation of three pathways for osmolyte efflux in human erythroleukemia cells.
【24h】

Characterisation of three pathways for osmolyte efflux in human erythroleukemia cells.

机译：人类红白血病细胞渗透渗出的三种途径的表征。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Cell volume decrease is a key step during differentiation of erythroid cells. This could arise from membrane transporter activation leading to a loss of cell osmolytes; however, the pathways involved are poorly understood. We have characterised Cl(-)-independent K(+) and (3)H-taurine efflux from the erythroleukemia cell line, K562. K(+) efflux (measured using (86)Rb(+)) from pre-loaded cells subjected to hypo-osmotic challenge demonstrated two phases, a rapid increase in K(+) efflux followed by a smaller slower increase. Swelling-activated taurine efflux only demonstrated a single phase. Both phases of K(+) efflux were significantly (P<0.05) blocked by anion channel inhibitor 5-nitro-2-(3-phenypropylamino)-benzoic acid (NPPB). However the antiestrogen, tamoxifen, only inhibited the slow late phase. The initial rapid phase had a higher IC(50) for NPPB inhibition than the slow phase, and was insensitive to protein kinases inhibitors KN-62, wortmannin and PD98059. For the slow K(+) efflux phase, the IC(50) for NPPB inhibition and the inhibition by KN-62, wortmannin, genistein or PD98059, were very similar to those measured for the hypo-osmotically-activated taurine efflux. With NPPB (100 microM) present, the slow K(+) efflux phase was further significantly decreased by the Ca(2+) chelator BAPTA-AM or by the Ca(2+)-activated K(+) channel blockers clotrimazole and charybdotoxin but not by apamin. Thus, at least 3 Cl(-)-independent pathways are involved: (a) a tamoxifen-sensitive and taurine-permeable anion channel; (b) a tamoxifen-insensitive and taurine-impermeable K(+) efflux pathway; and (c) a subtype of Ca(2+)-activated K(+) channel. Any or all of these could be involved in the cell volume decrease associated with differentiation in K562 cells.
机译：细胞体积的减少是红细胞分化过程中的关键步骤。这可能是由于膜转运蛋白的活化导致细胞渗透液的损失所致。但是，涉及的途径知之甚少。我们已经从红白血病细胞系，K562表征了不依赖Cl（-）的K（+）和（3）H-牛磺酸流出。来自经受低渗挑战的预加载细胞的K（+）外排（使用（86）Rb（+）测量）表现出两个阶段，K（+）外排快速增加，随后出现较小的缓慢增加。膨胀活化的牛磺酸流出仅表现出单相。阴离子通道抑制剂5-硝基-2-（3-苯丙氨基）-苯甲酸（NPPB）显着阻断了K（+）流出的两个阶段（P <0.05）。然而，抗雌激素他莫昔芬仅抑制缓慢的晚期。最初的快速阶段对NPPB的抑制作用要比慢速阶段的IC（50）高，并且对蛋白激酶抑制剂KN-62，渥曼青霉素和PD98059不敏感。对于缓慢的K（+）外排阶段，NPPB抑制作用的IC（50）和KN-62，渥曼青霉素，染料木黄酮或PD98059的抑制作用与低渗活化牛磺酸外排的测量结果非常相似。存在NPPB（100 microM）时，Ca（2+）螯合剂BAPTA-AM或Ca（2+）激活的K（+）通道阻滞剂克霉唑和甲藻毒素进一步显着降低了慢K（+）外排期但不是通过阿帕明。因此，至少涉及3个Cl（-）独立途径：（a）他莫昔芬敏感和牛磺酸可渗透的阴离子通道; （b）他莫昔芬不敏感且牛磺酸不渗透的K（+）外排途径; （c）Ca（2+）激活的K（+）通道的亚型。这些中的任何一个或全部可能与K562细胞分化相关的细胞体积减少有关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号