PDF(Pubmed)
Abstract：
Selectins are a group of Ca2+-dependent, transmembrane type I glycoproteins which attract cell adhesion and migration. E-selectin is exclusively expressed in endothelial cells, and its expression is strongly enhanced upon activation by pro-inflammatory cytokines. The interaction of E-selectin with its ligands on circulating leukocytes captures and slows them down, further facilitating integrin activation, firm adhesion to endothelial cells and transmigration to tissues. Oxidative stress induces endothelial cell injury, leading to aberrant expression of E-selectin. In addition, the elevated level of E-selectin is positively related to high risk of inflammation. Dysregulation of E-selectin has been found in several pathological conditions including acute kidney injury (AKI), pulmonary diseases, hepatic pathology, Venous thromboembolism (VTE). Deletion of the E-selectin gene in mice somewhat ameliorates these complications. In this review, we describe the mechanisms regulating E-selectin expression, the interaction of E-selectin with its ligands, the E-selectin physiological and pathophysiological roles, and the therapeutical potential of targeting E-selectin.
摘要：
选择素是一组依赖Ca2+的，吸引细胞粘附和迁移的跨膜I型糖蛋白。E-选择素仅在内皮细胞中表达，并且其表达在被促炎细胞因子激活时强烈增强。E-选择素与其配体在循环白细胞上的相互作用捕获并减慢它们，进一步促进整合素激活，牢固粘附于内皮细胞并迁移至组织。氧化应激诱导内皮细胞损伤，导致E-选择素的异常表达。此外,E-选择素水平升高与炎症的高风险呈正相关。在包括急性肾损伤（AKI）在内的几种病理状况中发现了E-选择素的失调，肺部疾病，肝脏病理学,静脉血栓栓塞症(VTE)。小鼠中E-选择素基因的缺失在一定程度上改善了这些并发症。在这次审查中,我们描述了调节E-选择素表达的机制，E-选择素与其配体的相互作用，E-选择素的生理和病理生理作用，以及靶向E-选择素的治疗潜力。
