Division of Ophthalmic Pathology, Department of Ophthalmology, University of Bonn, DE-53127 Bonn, Germany.
Pathobiology. 2013;80(5):245-51. doi: 10.1159/000347062. Epub 2013 Apr 27.
Vascular endothelial (VE) cadherin is a cell adhesion molecule localized at endothelial cell (EC) junctions. As a major component of endothelial adherens junctions, its main function is the maintenance and regulation of EC integrity. In the acute respiratory distress syndrome (ARDS), increased vascular permeability is a major mechanism in pulmonary edema and lung dysfunction. In this study, VE-cadherin expression was investigated in ARDS lungs and control tissue as well as in an ARDS cell culture model.
Lung specimens of patients with ARDS due to Gram-negative sepsis (n = 20; control lung tissue: n = 41) and cell cultures of human pulmonary microvascular ECs and human umbilical vein ECs stimulated with LPS, TNF-α and IFN-γ were stained with a VE-cadherin antibody. Staining intensity was semiquantitatively evaluated by conventional light and immunofluorescence microscopy.
VE-cadherin expression was statistically significantly reduced in the endothelium of all vessel types in ARDS lungs compared to control tissue. Cell cultures showing disrupted cellular borders confirmed these results.
Reduced expression of VE-cadherin has to be considered as a major mechanism of increased vessel permeability in ARDS. The previously described vessel-type-specific expression pattern of VE-cadherin in the human lung is not influenced by ARDS.
血管内皮（VE）钙黏蛋白是一种位于内皮细胞（EC）连接处的细胞黏附分子。作为内皮细胞黏附连接的主要组成部分，其主要功能是维持和调节 EC 的完整性。在急性呼吸窘迫综合征（ARDS）中，血管通透性增加是肺水肿和肺功能障碍的主要机制。在本研究中，研究了 ARDS 肺组织和对照组织以及 ARDS 细胞培养模型中的 VE-cadherin 表达。
用 VE-cadherin 抗体对革兰氏阴性菌脓毒症引起的 ARDS 患者的肺标本（n = 20；对照肺组织：n = 41）和人肺微血管内皮细胞和人脐静脉内皮细胞的 LPS、TNF-α 和 IFN-γ 刺激的细胞培养物进行染色。通过常规光镜和免疫荧光显微镜对半定量评估染色强度。
与对照组织相比，ARDS 肺组织中所有血管类型的内皮 VE-cadherin 表达均显著降低。显示细胞边界中断的细胞培养物证实了这些结果。
VE-cadherin 表达降低被认为是 ARDS 中血管通透性增加的主要机制。以前描述的 VE-cadherin 在人类肺中的血管类型特异性表达模式不受 ARDS 影响。
