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Different contributions of clathrin- and caveolae-mediated endocytosis of vascular endothelial cadherin to lipopolysaccharide-induced vascular hyperpermeability.网格蛋白和小窝介导的血管内皮钙黏蛋白内吞作用对脂多糖诱导的血管通透性增加的不同作用
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Actin-binding proteins differentially regulate endothelial cell stiffness, ICAM-1 function and neutrophil transmigration.肌动蛋白结合蛋白差异调节内皮细胞硬度、细胞间黏附分子-1 功能和中性粒细胞迁移。
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VE-cadherin Y685F knock-in mouse is sensitive to vascular permeability in recurrent angiogenic organs.血管内皮钙黏蛋白Y685F敲入小鼠对反复血管生成器官中的血管通透性敏感。
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黏附分子对血管通透性的调控

Control of vascular permeability by adhesion molecules.

作者信息

Sarelius Ingrid H, Glading Angela J

机构信息

University of Rochester; Department of Pharmacology and Physiology ; Rochester, NY USA.

出版信息

Tissue Barriers. 2015 Apr 3;3(1-2):e985954. doi: 10.4161/21688370.2014.985954. eCollection 2015.

DOI:10.4161/21688370.2014.985954
PMID:25838987
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4372019/
Abstract

Vascular permeability is a vital function of the circulatory system that is regulated in large part by the limited flux of solutes, water, and cells through the endothelial cell layer. One major pathway through this barrier is via the inter-endothelial junction, which is driven by the regulation of cadherin-based adhesions. The endothelium also forms attachments with surrounding proteins and cells via 2 classes of adhesion molecules, the integrins and IgCAMs. Integrins and IgCAMs propagate activation of multiple downstream signals that potentially impact cadherin adhesion. Here we discuss the known contributions of integrin and IgCAM signaling to the regulation of cadherin adhesion stability, endothelial barrier function, and vascular permeability. Emphasis is placed on known and prospective crosstalk signaling mechanisms between integrins, the IgCAMs- ICAM-1 and PECAM-1, and inter-endothelial cadherin adhesions, as potential strategic signaling nodes for multipartite regulation of cadherin adhesion.

摘要

血管通透性是循环系统的一项重要功能,在很大程度上由溶质、水和细胞通过内皮细胞层的有限通量来调节。穿过这一屏障的一条主要途径是通过内皮细胞间连接,其由基于钙黏蛋白的黏附调节驱动。内皮细胞还通过两类黏附分子,即整合素和免疫球蛋白超家族细胞黏附分子(IgCAMs),与周围的蛋白质和细胞形成附着。整合素和IgCAMs可促进多个下游信号的激活,这些信号可能会影响钙黏蛋白的黏附。在此,我们讨论整合素和IgCAM信号传导对钙黏蛋白黏附稳定性、内皮屏障功能和血管通透性调节的已知作用。重点关注整合素、IgCAMs(细胞间黏附分子-1和血小板内皮细胞黏附分子-1)与内皮细胞间钙黏蛋白黏附之间已知的和潜在的串扰信号传导机制,将其作为钙黏蛋白黏附多方面调节的潜在战略信号节点。