首页> 外文期刊>American Journal of Physiology >p38 MAPK activation coupled to endocytosis is a determinant of endothelial monolayer integrity.
【24h】

p38 MAPK activation coupled to endocytosis is a determinant of endothelial monolayer integrity.

机译:与内吞作用偶联的p38 MAPK激活是内皮单层完整性的决定因素。

获取原文
获取原文并翻译 | 示例
           

摘要

We show in rat lung microvessel endothelial cells (RLMVEC) that endocytosis is a critical determinant of activation of mitogen-activated protein kinase (MAPK) and thereby regulates endothelial monolayer integrity. In RLMVEC grown in serum-free medium, we observed that albumin supplementation induced the phosphorylation of p38 MAPK within 30 min, which persisted for up to 2 h. Engagement of the endocytic machinery regulated the activation of p38 MAPK that contributed to endothelial cell proliferation and reduction of apoptosis. We also observed an interaction between the caveolar protein caveolin-1 and p38 MAPK with reciprocal coimmunoprecipitation assays and colocalization using double-label immunofluorescence staining. Knockdown of caveolin-1 expression with small interfering RNA significantly reduced endocytosis and activation of p38 MAPK and interfered with the ability of endothelial cells to form a confluent monolayer. Thus caveolae-mediated endocytosis and concomitant activation of p38 MAPK may help to maintain endothelial monolayer integrity by signaling proliferation and survival of endothelial cells.
机译:我们在大鼠肺微血管内皮细胞(RLMVEC)中显示,胞吞作用是促有丝分裂原激活的蛋白激酶(MAPK)激活的关键决定因素,从而调节内皮单层完整性。在无血清培养基中生长的RLMVEC中,我们观察到补充白蛋白可在30分钟内诱导p38 MAPK磷酸化,并持续2 h。内吞机制的参与调节了p38 MAPK的激活,从而促进了内皮细胞的增殖和凋亡的减少。我们还观察到海绵体蛋白caveolin-1和p38 MAPK之间的相互作用与相互免疫共沉淀测定和使用双标记免疫荧光染色的共定位。用小干扰RNA敲低小窝蛋白1的表达可显着降低内吞作用和p38 MAPK的激活,并干扰内皮细胞形成融合单层的能力。因此,caveolae介导的内吞作用和p38 MAPK的伴随活化可能通过信号化内皮细胞的增殖和存活来帮助维持内皮单层完整性。

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