Platelet endothelial cell adhesion molecule-1 (PECAM1) plays a critical role in the maintenance of human vascular endothelial barrier function

被引:23
|
作者
Ren, Qi [1 ,2 ]
Ren, Limin [3 ]
Ren, Changjie [2 ]
Liu, Xuefei [1 ]
Dong, Chun [2 ]
Zhang, Xinghua [1 ]
机构
[1] Shandong Univ, Shandong Prov Hosp, Dept Cardiol, Jinan 250021, Shandong, Peoples R China
[2] Jining 1 Peoples Hosp, Dept Cardiol, Jining 272011, Shandong, Peoples R China
[3] Zoucheng Peoples Hosp, Dept Neurosurg, Jining 273500, Shandong, Peoples R China
关键词
platelet endothelial cell adhesion molecule-1; tight junction; tight junction associated protein; endothelium; barrier function; PERMEABILITY; EXPRESSION; INFLAMMATION; CLAUDIN-5; JUNCTIONS;
D O I
10.1002/cbf.3155
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cardiovascular endothelial barrier dysfunction is associated with a number of cardiovascular diseases. This study aims to investigate the role of platelet endothelial cell adhesion molecule-1 (PECAM1) in the maintenance of the vascular endothelial barrier integrate. Human umbilical vein endothelial cells (HUVECs) were cultured into monolayers using as an in vitro model to assess the endothelial barrier function. Knockdown of the gene of PECAM1 markedly reduced the transendothelial resistance and increased the permeability of the HUVEC monolayers. From the wild HUVECs, we detected a complex of PECAM1, claudin1, occluding and endothelial cell selective adhesion molecule (ESAM); such a complex was not detected in the PECAM1-deficient HUVECs. Knockdown of either claudin1, or occludin, or ESAM, did not affect the formation of the tight junction (TJ) complex. Exposure to recombinant interleukin (IL)-13 inhibited the expression of PECAM1 and down-regulated the HUVEC monolayer barrier function. PECAM1 plays an important role in the formation of TJ complex. Copyright (C) 2015 John Wiley & Sons, Ltd.
引用
收藏
页码:560 / 565
页数:6
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