• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell biology international. >C-reactive protein increases F-actin assembly and cortical distribution with resultant loss of lamellipod formation in human neutrophils.
【24h】

C-reactive protein increases F-actin assembly and cortical distribution with resultant loss of lamellipod formation in human neutrophils.

机译：C反应蛋白会增加F-肌动蛋白的组装和皮质分布，从而导致人类嗜中性粒细胞中lamellipod形成的损失。

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

C-reactive protein (CRP) inhibits neutrophil movement through a p38 MAP kinase pathway. We hypothesized that CRP altered F-actin content and distribution on human neutrophils as a means of inhibiting movement. CRP produced simultaneous increased F-actin and decreased G-actin levels. CRP increased F-actin levels in a concentration-dependent manner once a threshold (>100 microg/ml) was reached, and transiently increased F-actin (peak levels at 2.5 and 10 min) that returned to baseline by 30 min. Confocal microscopy of neutrophils revealed that fMLP provoked acquisition of a migratory phenotype as evidenced by the appearance of F-actin rich lamellipods. In contrast, CRP caused neutrophil rounding, prevented lamellipod formation and shifted F-actin from the cytoskeleton to the cortex. The p38 MAP kinase inhibitor, SB203580, produced a similar effect on neutrophil shape. Concentrations of SB203580 that dramatically decreased p38 activity in neutrophils also caused round cell morphology and cortical F-actin distribution. Since CRP inhibits p38 MAP kinase and p38 blockade leads to actin polymerization and prevention of lamellipod formation, it is concluded that round morphology and loss of lamellipod formation result from CRP inhibition of p38 MAP kinase. Understanding the signal transduction of CRP prevention of lamellipod formation will aid in the development of therapeutic agents against neutrophil-associated inflammatory disease.
机译：C反应蛋白（CRP）通过p38 MAP激酶途径抑制嗜中性粒细胞运动。我们假设CRP改变了人类嗜中性粒细胞中F-肌动蛋白的含量和分布，从而抑制了运动。 CRP同时产生F-肌动蛋白升高和G-肌动蛋白水平降低。一旦达到阈值（> 100 microg / ml），CRP就会以浓度依赖的方式增加F-肌动蛋白水平，并短暂增加F-肌动蛋白（在2.5和10分钟时的峰值水平），并在30分钟后恢复基线。中性粒细胞的共聚焦显微镜检查显示，fMLP引起了迁移性表型的获得，这是由富含F-肌动蛋白的片状脂质体的出现所证明的。相反，CRP导致中性粒细胞变圆，阻止了lamellipod的形成，并使F-肌动蛋白从细胞骨架转移到了皮质。 p38 MAP激酶抑制剂SB203580对中性粒细胞的形状产生了相似的作用。 SB203580的浓度会显着降低中性粒细胞中p38的活性，还会引起圆形细胞形态和皮质F-肌动蛋白分布。由于CRP抑制p38 MAP激酶，而p38阻断导致肌动蛋白聚合并阻止lamellipod的形成，因此可以得出结论，CRP抑制p38 MAP激酶可导致圆形形态和lamellipod形成的丧失。了解CRP预防lamellipod形成的信号转导将有助于开发针对中性粒细胞相关性炎性疾病的治疗剂。

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