Differentiation of endothelial barrier function during normal angiogenesis requires homotypic VE-cadherin adhesion.
Endothelial cells express two principal cadherins: VE-cadherin and N-cadherin. We established previously that only VE-cadherin expression was increased during differentiation of barrier function by angiogenic endothelium of the chick chorioallantoic membrane (CAM). Presently anti-VE-cadherin mAb, applied to the CAM at day 4.5 of gestation, served to inhibit the abrupt reduction of macromolecular extravasation that occurs normally at day 5.0. Neither anti-N-cadherin nor nonimmune IgG, on the other hand, prevented this temporal decrease of endothelial permeability. Despite the differential permeability responses, morphometric evaluations defined a reduction of mean paracellular cleft width after the application of either anti-VE-cadherin or anti-N-cadherin. Hence, alteration of molecular sieving characteristics within the junctional clefts, rather than modification of cleft dimensions; likely served as the principal modulator of macromolecular extravasation after inhibition of homotypic VE-cadherin adhesion. These results provide support to the concept that VE-cadherin contributes to the normal differentiation of endothelial barrier function during CAM angiogenesis in vivo.
DeFouw
L M
LM
Department of Anatomy, Cell Biology and Injury Sciences UMDNJ-New Jersey Medical School, Newark 07103, USA.
DeFouw
D O
DO
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D015703:Antigens, CD; D015820:Cadherins / Q000276:immunology / Q000502:physiology*; D002199:Capillary Permeability; D002448:Cell Adhesion; D002642:Chick Embryo; D004730:Endothelium, Vascular / Q000196:embryology / Q000502:physiology* / Q000648:ultrastructure; D005321:Extraembryonic Membranes / Q000502:physiology / Q000648:ultrastructure; D018919:Neovascularization, Physiologic; D000099152:Cadherin 5
D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015820:Cadherins; D000099152:Cadherin 5