• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Role of connexin 43 in vascular hyperpermeability and relationship to Rockl-MLC_(20) pathway in septic rats
【24h】

Role of connexin 43 in vascular hyperpermeability and relationship to Rockl-MLC_(20) pathway in septic rats

机译：Connexin 43在血管超透性中的作用和岩体大鼠Rockl-MLC_（20）途径的关系

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

Connexin (Cx)43 has been shown to participate in several cardiovascular diseases. Increased vascular permeability is a common and severe complication in sepsis or septic shock. Whether or not Cx43 takes part in the regulation of vascular permeability in severe sepsis is not known, and the underlying mechanism has not been described. With cecal ligation and puncture-induced sepsis in rats and lipopolysaccharide (LPS)-treated vascular endothelial cells (VECs) from pulmonary veins, the role of Cx43 in increased vascular permeability and its relationship to the RhoA/Rock1 pathway were studied. It was shown that vascular permeability in the lungs, kidneys, and mesentery in sepsis rats and LPS-stimulated monolayer pulmonary vein VECs was significantly increased and positively correlated with the increased expression of Cx43 and Rock1 in these organs and cultured pulmonary vein VECs. The connexin inhibitor carbenoxolone (10 mg/kg iv) and the Rockl inhibitor Y-27632 (2 mg/kg iv) alleviated the vascular leakage of lung, mesentery, and kidney in sepsis rats. Overexpressed Cx43 increased the phosphorylation of 20-kDa myosin light chain (MLC_(20)) and the expression of Rockl and increased the vascular permeability and decreased the transendothelial electrical resistance of pulmonary vein VECs. Cx43 RNA interference decreased the phosphorylation of MLC_(20) and the expression of Rockl and decreased LPS-stimulated hyperpermeability of cultured pulmonary vein VECs. The Rockl inhibitor Y-27632 alleviated LPS- and overexpressed Cx43-induced hyperpermeability of monolayer pulmonary vein VECs. This report shows that Cx43 participates in the regulation of vascular permeability in sepsis and that the mechanism is related to the Rock1-MLC_(20) phosphorylation pathway.
机译：Connexin（CX）43已被证明参与几种心血管疾病。血管渗透性增加是败血症或脓毒症休克的常见和严重的复杂性。 CX43是否参与严重败血症中血管渗透性的调节尚不清楚，并且尚未描述潜在机制。在大鼠和脂多糖（LPS） - 治疗的血管内皮细胞（VECs）中，来自肺静脉的血管结扎和穿刺诱导的脓毒症，研究了CX43在血管渗透性增加的作用及其与RhoA / Rock1途径的关系。结果表明，血管大鼠和LPS刺激的单层肺静脉VECS中肺部，肾脏和肠膜内的血管渗透性显着增加，与这些器官和培养的肺静脉VECS中的CX43和ROCK1的表达呈正相关。 Connexin抑制剂碳氧酮（10mg / kg IV）和Rock1抑制剂Y-27632（2mg / kg IV）缓解了败血症大鼠肺癌，肠系膜和肾脏的血管泄漏。过表达的CX43增加了20-KDA肌球蛋白轻链的磷酸化（MLC_（20））和ROCK1的表达并增加血管渗透性并降低肺静脉VECs的常旧电阻。 CX43 RNA干扰降低了MLC_（20）的磷酸化和ROCK1的表达并降低了培养的肺静脉VECs的LPS刺激的超甲型。 Rockl抑制剂Y-27632缓解了LPS-和过表达的CX43诱导的单层肺静脉VECS的高透析性。本报告显示CX43参与败血症血管渗透性的调节，并且该机制与Rock1-MLC_（20）磷酸化途径有关。

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