Moll T, Dejana E, Vestweber D
Institute of Cell Biology, Zentrum für die Molekularbiologie der Entzündung, University of Münster, Germany.
J Cell Biol. 1998 Jan 26;140(2):403-7. doi: 10.1083/jcb.140.2.403.
It has been recently proposed that adhesion of polymorphonuclear cells (PMNs) to human umbilical vein endothelial cells leads to the disorganization of the vascular endothelial cadherin-dependent endothelial adherens junctions. Combined immunofluorescence and biochemical data suggested that after adhesion of PMNs to the endothelial cell surface, beta-catenin, as well as plakoglobin was lost from the cadherin/catenin complex and from total cell lysates. In this study we present data that strongly suggest that the adhesion-dependent disappearance of endothelial catenins is not mediated by a leukocyte to endothelium signaling event, but is due to the activity of a neutrophil protease that is released upon detergent lysis of the cells.
最近有人提出,多形核细胞(PMN)与人脐静脉内皮细胞的黏附会导致血管内皮钙黏蛋白依赖性内皮黏附连接的紊乱。联合免疫荧光和生化数据表明,PMN黏附于内皮细胞表面后,β-连环蛋白以及桥粒斑蛋白从钙黏蛋白/连环蛋白复合物和总细胞裂解物中消失。在本研究中,我们提供的数据有力地表明,内皮连环蛋白依赖黏附的消失不是由白细胞向内皮细胞的信号转导事件介导的,而是由于细胞经去污剂裂解后释放的中性粒细胞蛋白酶的活性所致。