Abstract
Endothelial cell–cell adhesion within the wall of the vasculature controls a range of physiological processes, such as growth, integrity and barrier function. The adhesive properties of endothelial cells are tightly controlled by a complex cascade of signals transmitted from the surrounding environment or from within the cells themselves, with the dynamic nature of cellular adhesion and the regulating signalling networks now beginning to be appreciated. Here, we summarise the current knowledge of the mechanisms controlling endothelial cell–cell adhesion in the developing and mature blood vasculature.
Highlights
Blood vessels form complex branched networks consisting of arteries, capillaries and veins that supply oxygen and nutrients to all body tissues [1]
The regulation of cell–cell adhesion is critical during blood vessel formation and function, as cells within the vessel wall need to be able to move around each other while maintaining a functional vascular barrier
Summary
Blood vessels form complex branched networks consisting of arteries, capillaries and veins that supply oxygen and nutrients to all body tissues [1]. Vasculogenesis, angiogenesis and vascular remodelling are all highly dynamic processes, in which the adhesion of endothelial cells within the vessel wall is tightly controlled This allows for cells to both grow and move past one another during sprouting, while maintaining a functional vascular barrier to prevent leakage from vessels. During early vasculogenesis in the mouse, endothelial cell precursors arise at embryonic day 8 and subsequently assemble into an immature network of vascular cords These precursors differentiate to become lumenised, allowing for blood to pass through. The generation of active Cdc is regulated by Rasip (Ras-interacting protein 1), resulting in contractile nonmuscle myosin II (NMII) and F-actin pulling adhesion complexes away from the cell–cell contacts on the apical surface [12,13] This is similar to what is observed during sprouting angiogenesis, where disruption of the interaction between actin and VE-cadherin results in a failure of lumen formation and maintenance [14]. Rasip is required for formation of the lumen during vasculogenesis, and for the maintenance of the lumenised vasculature during development [15,16]
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