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首页> 外文期刊>Frontiers in Cell and Developmental Biology >Differential regulation of LPS-mediated VE-cadherin disruption in human endothelial cells and the underlying signaling pathways: A mini review
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Differential regulation of LPS-mediated VE-cadherin disruption in human endothelial cells and the underlying signaling pathways: A mini review

机译：LPS介导的人内皮细胞中VE-钙粘蛋白破坏的差异调节及其潜在的信号传导途径：综述

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摘要

Endothelial cells lining the inner vascular wall form a monolayer that contributes to the selective permeability of endothelial barrier. This selective permeability is mainly regulated by an endothelium-specific adherens junctional protein, known as vascular endothelial-cadherin (VE-cadherin). In endothelial cells, the adherens junction comprises of VE-cadherin and its associated adhesion molecules such as p120, α-catenin and β-catenin, in which α-catenin links cytoplasmic tails of VE-cadherin to actin cytoskeleton through β-catenin. Proinflammatory stimuli such as lipopolysaccharide (LPS) are capable of attenuating vascular integrity through the disruption of VE-cadherin adhesion in endothelial cells. To date, numerous studies demonstrated the disruption of adherens junction as a result of phosphorylation-mediated VE-cadherin disruption. However, the outcomes from these studies were inconsistent and non-conclusive as different cell fractions were used to examine the effect of LPS on the disruption of VE-cadherin. By using Western Blot, some studies utilized total protein lysate and reported decreased protein expression while some studies reported unchanged expression. Other studies which used membrane and cytosolic fractions of protein extract demonstrated decreased and increased VE-cadherin expression, respectively. Despite the irregularities, the results of immunofluorescence staining are consistent with the formation of intercellular gap. Besides that, the overall underlying disruptive mechanisms of VE-cadherin remain largely unknown. Therefore, this mini review will focus on cell fractions used in different studies with different human endothelial cell models, and relate them to the results obtained in Western Blot and immunofluorescence staining in order to give some insights into the overall mechanisms of LPS-induced VE-cadherin disruption and address the discrepancy in VE-cadherin expression.
机译：衬在血管内壁上的内皮细胞形成单层，有助于内皮屏障的选择性渗透。这种选择性的通透性主要是由称为血管内皮钙粘蛋白（VE-cadherin）的内皮特异性粘附连接蛋白调节的。在内皮细胞中，粘附连接由VE-钙粘蛋白及其相关的粘附分子（例如p120，α-catenin和β-catenin）组成，其中α-catenin通过β-catenin将VE-cadherin的细胞质尾部连接至肌动蛋白细胞骨架。促炎性刺激（例如脂多糖（LPS））能够通过破坏内皮细胞中的VE-钙黏着蛋白粘附来削弱血管完整性。迄今为止，大量研究表明，由于磷酸化介导的VE-钙黏着蛋白破坏，粘附连接的破坏。但是，这些研究的结果不一致且不确定，因为使用了不同的细胞部分来检查LPS对VE-钙粘蛋白破坏的影响。通过使用蛋白质印迹法，一些研究利用了总蛋白裂解物，并报告了蛋白表达下降，而一些研究则报告了未改变的表达。使用蛋白质提取物的膜部分和胞质部分的其他研究表明，VE-钙黏着蛋白表达分别降低和增加。尽管有这些不规则之处，但免疫荧光染色的结果与细胞间间隙的形成是一致的。除此之外，VE-钙粘着蛋白的整体潜在破坏机制仍然未知。因此，本篇小型综述将重点讨论用于不同人类内皮细胞模型的不同研究中使用的细胞部分，并将它们与Western Blot和免疫荧光染色中获得的结果相关联，以便对LPS诱导的VE-钙粘蛋白破坏和解决VE-钙粘蛋白表达的差异。

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