• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>other >Fibrin-Induced Epithelial-to-Mesenchymal Transition of Peritoneal Mesothelial Cells as a Mechanism of Peritoneal Fibrosis: Effects of Pentoxifylline
【2h】

Fibrin-Induced Epithelial-to-Mesenchymal Transition of Peritoneal Mesothelial Cells as a Mechanism of Peritoneal Fibrosis: Effects of Pentoxifylline

机译：纤维蛋白 - 诱导上皮 - 间充质腹膜间皮细胞作为腹膜纤维化的机理的过渡：己酮可可碱的影响

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Excessive fibrin deposition in the peritoneum is thought to be involved in the development of encapsulating peritoneal sclerosis (EPS), an important cause of morbidity and mortality in peritoneal dialysis patients. We investigated fibrin-induced epithelial-to-mesenchymal transition (EMT) of peritoneal mesothelial cells (PMCs) as a possible mechanism of fibrin involvement in EPS. In vitro, fibrin overlay of PMCs altered their morphology; increased α-smooth muscle actin, fibronectin, fibroblast specific protein-1, and αvβ3 integrin expression; and decreased cytokeratin 18 and E-cadherin expression. Fibrin overlay also increased focal adhesion kinase and Src kinase phosphorylation. Fibrin-induced changes were inhibited by treating the cells with αvβ3 integrin antibody or pentoxifylline (PTX). In a rat model, intraperitoneal injection of Staphylococcus aureus and fibrinogen induced severe EPS features, which were attenuated by PTX treatment. PTX-treated rats also showed preserved peritoneal ultrafiltration function and lower concentrations of cytokines than the untreated rats. S. aureus- and fibrinogen-injected rats had higher percentage of cytokeratin-positive cells in the omentum fibrotic tissue than controls; this was also reduced by PTX treatment. Our results suggest that fibrin induces EMT of PMCs by engaging αvβ3 integrin and activating associated kinases. Our EPS animal model showed that fibrin-induced EMT was involved in the pathogenesis of peritoneal fibrosis and was inhibited by PTX.
机译：腹膜中过多的纤维蛋白沉积被认为与包膜性腹膜硬化（EPS）的发展有关，后者是腹膜透析患者发病和死亡的重要原因。我们调查了纤维蛋白诱导的腹膜间皮细胞（PMCs）的上皮-间质转化（EMT）作为纤维蛋白参与EPS的可能机制。在体外，PMC的纤维蛋白覆盖改变了它们的形态。增加α-平滑肌肌动蛋白，纤连蛋白，成纤维细胞特异性蛋白-1和αvβ3整联蛋白的表达；并降低细胞角蛋白18和E-钙粘蛋白的表达。纤维蛋白覆盖还增加了粘着斑激酶和Src激酶的磷酸化。通过用αvβ3整联蛋白抗体或己酮可可碱（PTX）处理细胞可抑制血纤蛋白诱导的变化。在大鼠模型中，腹膜内注射金黄色葡萄球菌和纤维蛋白原可导致严重的EPS特征，而PTX处理可减轻这些特征。与未经处理的大鼠相比，经PTX处理的​​大鼠还表现出了腹膜超滤功能的维持和较低的细胞因子浓度。注射金黄色葡萄球菌和纤维蛋白原的大鼠在大网膜纤维化组织中的细胞角蛋白阳性细胞百分比高于对照组。 PTX处理也减少了这种情况。我们的结果表明，纤维蛋白通过与αvβ3整联蛋白结合并激活相关激酶来诱导PMC的EMT。我们的EPS动物模型显示，纤维蛋白诱导的EMT参与腹膜纤维化的发病机制，并被PTX抑制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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