Nan Weijin, He Yuxi, Wang Shurong, Zhang Yan
Department of Ophthalmology, The Second Hospital of Jilin University, Changchun, China.
Department of Ophthalmology, China-Japan Union Hospital of Jilin University, Changchun, China.
Front Physiol. 2023 Aug 2;14:1234104. doi: 10.3389/fphys.2023.1234104. eCollection 2023.
Vascular endothelial (VE)-cadherin, an endothelium-specific adhesion protein, is found in the junctions between endothelial cells (ECs). It's crucial to maintain the homogeneity of ECs. Keeping and controlling the contact between ECs is essential. In addition to its adhesive function, VE-cadherin plays important roles in vascular development, permeability, and tumour angiogenesis. Signal transfer, cytoskeletal reconstruction, and contractile integrating, which are crucial for constructing and maintaining monolayer integrity as well as for repair and regeneration, are the foundation of endothelial cell (EC) junctional dynamics. The molecular basis of adhesion junctions (AJs), which are closely related and work with actin filaments, is provided by the VE-cadherin-catenin complex. They can activate intracellular signals that drive ECs to react or communicate structural changes to junctions. An increasing number of molecules, including the vascular endothelial growth factor receptor 2 (VEGFR2) and vascular endothelial protein tyrosine phosphatase (VE-PTP), have been connected to VE-cadherin in addition to the conventional VE-cadherin-catenin complex. This review demonstrates significant progress in our understanding of the molecular mechanisms that affect VE-cadherin's function in the regulation of EC behaviour during angiogenesis. The knowledge of the molecular processes that control VE-cadherin's role in the regulation of EC behaviour during angiogenesis has recently advanced, as shown in this review.
血管内皮(VE)-钙黏蛋白是一种内皮细胞特异性黏附蛋白,存在于内皮细胞(EC)之间的连接处。它对于维持内皮细胞的同质性至关重要。保持和控制内皮细胞之间的接触至关重要。除了其黏附功能外,VE-钙黏蛋白在血管发育、通透性和肿瘤血管生成中也发挥着重要作用。信号传递、细胞骨架重建和收缩整合是内皮细胞(EC)连接动力学的基础,对于构建和维持单层完整性以及修复和再生至关重要。VE-钙黏蛋白-连环蛋白复合物为与肌动蛋白丝密切相关并协同作用的黏附连接(AJs)提供了分子基础。它们可以激活细胞内信号,驱动内皮细胞做出反应或将结构变化传递给连接处。除了传统的VE-钙黏蛋白-连环蛋白复合物外,越来越多的分子,包括血管内皮生长因子受体2(VEGFR2)和血管内皮蛋白酪氨酸磷酸酶(VE-PTP),已与VE-钙黏蛋白相关联。本综述展示了我们在理解影响VE-钙黏蛋白在血管生成过程中调节内皮细胞行为功能的分子机制方面取得的重大进展。如本综述所示,最近在控制VE-钙黏蛋白在血管生成过程中调节内皮细胞行为作用的分子过程方面的知识有了进展。