...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Brain natriuretic peptide modulates the delayed rectifier outward K(+) current and promotes the proliferation of mouse Schwann cells.
【24h】

Brain natriuretic peptide modulates the delayed rectifier outward K(+) current and promotes the proliferation of mouse Schwann cells.

机译：脑利钠肽调节的延迟整流器外K(+)当前和促进鼠雪旺细胞扩散。

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

Brain natriuretic peptide (BNP) may act as a neuromodulator via its associated receptors (natriuretic peptide receptors, NPRs) in the central nervous system (CNS), but few studies have reported its activity in the peripheral nervous system (PNS). In this study, we observed that BNP increased the tetraethylammonium chloride (TEA)-sensitive delayed rectifier outward potassium current (I(K)) in mouse Schwann cells (SCs) using whole-cell recording techniques. At concentrations of 1-100 nM, BNP reversibly activated I(K) in a dose-dependent manner, with modulating its steady-state activation and inactivation properties. The effect of BNP on I(K) was abolished by preincubation with the specific antagonist of NPR-A, and could not be mimicked by application of NPR-C agonist. These results were supported by immunocytochemical findings indicating that NPR-A was expressed in SCs. The application of 8-Br-guanosine 3',5'-monophosphate (8-Br-cGMP) mimicked the effect of BNP on I(K), but BNP was unable to further increase I(K) after the application of cyclic guanosine monophosphate (cGMP). Genistein blocked I(K) and also completely eliminated the effects of BNP and cGMP on I(K). The selective K(V)2.1 subunit blocker, Jingzhaotoxin-III (JZTX-III), reduced I(K) amplitude by 30%, but did not abolish the increase effect of BNP on I(K) amplitude. In addition, BNP significantly stimulated SCs proliferation and this effect could be partly inhibited by TEA. Together these results suggest that BNP modulated I(K) probably via cGMP- and tyrosine kinase-dependent pathways by activation of NPR-A. This effect of BNP on I(K) in SCs might partly explain its effect on cell proliferation.
机译：脑利钠肽(BNP)可能充当神经调质通过其受体有关(利钠肽受体,npr)中枢神经系统(CNS),但很少有人研究有报道其外围的活动吗神经系统(pn)。法国巴黎银行增加了四乙铵氯化(茶)敏感的延迟整流外向钾电流(I (K))在鼠雪旺使用全细胞记录细胞(SCs)技术。可逆地激活我在存在剂量依赖的相关性(K)与调制方式,其稳态激活和失活特性。巴黎银行对我的影响(K)被废除预培养的具体对手NPR-A,无法模仿的应用程序NPR-C受体激动剂。采用免疫研究结果表明NPR-A在SCs表示。8-Br-guanosine 3 ', 5 '一磷酸(8-Br-cGMP)模仿法国巴黎在我(K)的影响,但法国巴黎无法进一步提高后,我(K)环鸟苷酸的应用(cGMP)。完全消除法国巴黎银行和cGMP的影响在我(K)。Jingzhaotoxin-III (JZTX-III),减少了我(K)幅度为30%,但没有废除增加法国对我的影响(K)振幅。此外,法国巴黎大大刺激了SCs增殖,这种效应可能部分被茶。,法国巴黎调制通过cGMP,我可能(K)酪氨酸kinase-dependent通路被激活NPR-A。部分解释其对细胞增殖的影响。

著录项

相似文献

  • 外文文献
  • 中文文献
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