Fig. 2.

Schematic diagram showing how VEGF may disrupt adherens junctions, the major regulator of paracellular permeability in human placental exchange vessels. Occupation of VEGFR-2 by VEGF may lead to autophosphorylation of VE-cadherin with loss of anchorage to actin, declustering and translocation of VE-cadherin and β-catenin. This would alter cleft dimension and paracellular filter properties, affecting rate of transfer and allowing transport of larger hydrophilic proteins.