VE-cadherin and claudin-5: it takes two to tango

TL;DR

This paper explores the interaction between VE-cadherin and claudin-5 in endothelial junctions, revealing how VE-cadherin influences claudin-5 expression through regulation of FoxO1 and catenin, highlighting a crosstalk mechanism.

Contribution

It uncovers a novel crosstalk mechanism where VE-cadherin controls claudin-5 expression via FoxO1 and catenin regulation in endothelial cells.

Findings

VE-cadherin prevents nuclear accumulation of FoxO1 and catenin.

This regulation promotes claudin-5 expression.

A crosstalk mechanism between adherens and tight junctions is proposed.

Abstract

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.