  Endothelial barrier function requires the adhesive activity of VE-cadherin
and claudin-5, which are key components of adherens and tight endothelial
junctions, respectively. Emerging evidence suggests that VE-cadherin controls
claudin-5 expression by preventing the nuclear accumulation of FoxO1 and
-catenin, which repress the claudin-5 promoter. This indicates that a crosstalk
mechanism operates between these junctional structures.
