• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Endothelium: Journal of endothelial cell research >Role of ligand-specific integrins in endothelial cell alignment and elongation induced by cyclic strain.
【24h】

Role of ligand-specific integrins in endothelial cell alignment and elongation induced by cyclic strain.

机译：配体特异性整合素在循环应变诱导的内皮细胞排列和伸长中的作用。

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

Ligand-specific integrins are thought to play a critical role in regulating multiple biological processes. However, the mechanisms by which ligand-specific integrins mediate external stimuli and activate intracellular signaling pathways remain to be elucidated. The aim of this study was to clarify the role of ligand-specific integrins in the morphological changes induced by cyclic strain (CS) via the p38 mitogen-activated protein kinase (p38 MAPK) pathway. Endothelial cells (ECs) were cultured on collagen (a ligand for integrin alpha 2 beta1, but not for alpha 5 and beta 4)-coated flexible plates and incubated for 24 h with or without anti-alpha2 integrin antibody (anti-alpha2), anti-alpha5, anti-beta1, or anti-beta4. ECs were then subjected to 15.6% average CS at 60 cycles/min up to 24 h. After exposure to CS, the cell shape index (defined as (4pi x cell area)/(cell perimeter)(2)), the cell orientation angle, and activation of p38 MAPK were assessed. ECs in the absence of integrin-blocking antibodies were elongated and aligned in response to CS. Anti-alpha 2 and anti-beta1 abolished both morphological changes of ECs as well as the activation of p38 MAPK. In contrast, anti-alpha 5 and anti-beta 4 inhibited neither morphological changes of ECs nor the activation of p38 MAPK. Our results indicate that ligand-specific integrins play a crucial role in the morphological changes of ECs induced by CS via the p38 MAPK pathway.
机译：配体特异性整合素被认为在调节多种生物过程中起着关键作用。但是，配体特异性整联蛋白介导外部刺激并激活细胞内信号传导途径的机制尚待阐明。这项研究的目的是阐明配体特异性整合素在通过p38促分裂原活化蛋白激酶（p38 MAPK）途径由循环菌株（CS）诱导的形态变化中的作用。内皮细胞（ECs）在胶原蛋白（整联蛋白alpha 2 beta1的配体，而不是alpha 5和beta 4的配体）上培养，并在有或没有抗alpha2整联蛋白抗体（anti-alpha2）的情况下孵育24小时，抗alpha5，抗beta1或抗beta4。然后，以60个周期/分钟的速度，对EC进行平均15.6％的CS，直至24小时。暴露于CS后，评估细胞形状指数（定义为（4pi x细胞面积）/（细胞周长）（2）），细胞方向角和p38 MAPK的激活。缺少整合素阻断抗体的EC被拉长并响应CS排列。抗α2和抗β1消除了EC的形态变化以及p38 MAPK的激活。相反，抗α5和抗β4既不抑制EC的形态变化，也不抑制p38 MAPK的激活。我们的结果表明，配体特异性整合素在CS通过p38 MAPK途径诱导的EC形态变化中起着关键作用。

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