|ZFIN ID: ZDB-PUB-170308-11|
Distinct and redundant functions of Esam and VE-cadherin during vascular morphogenesis
Sauteur, L., Affolter, M., Belting, H.G.
|Source:||Development (Cambridge, England) 144(8): 1554-1565 (Journal)|
|Registered Authors:||Affolter, Markus, Belting, Heinz-Georg Paul (Henry), Sauteur, Loïc|
|Keywords:||Esam, VE-cadherin, anastomosis, angiogenesis, cdh5, cell adhesion, cell contact formation, endothelial cell, morphogenesis, zebrafish|
|PubMed:||28264837 Full text @ Development|
Sauteur, L., Affolter, M., Belting, H.G. (2017) Distinct and redundant functions of Esam and VE-cadherin during vascular morphogenesis. Development (Cambridge, England). 144(8):1554-1565.
ABSTRACTThe cardiovascular system forms during early embryogenesis and adapts to embryonic growth by sprouting angiogenesis and vascular remodeling. These processes require fine-tuning of cell-cell adhesion to maintain and re-establish endothelial contacts, while allowing cell motility. We have compared the contribution of two endothelial cell-specific adhesion proteins, VE-cadherin (VE-cad/Cdh5) and Esama (endothelial cell-selective adhesion molecule a), during angiogenic sprouting and blood vessel fusion (anastomosis) in the zebrafish embryo by genetic analyses. Different combinations of mutant alleles can be placed into a phenotypic series with increasing defects in filopodial contact formation. Contact formation in esama mutants appears similar to wild type, whereas esama-/-; ve-cad+/- and ve-cad single mutants exhibit intermediate phenotypes. The lack of both proteins interrupts filopodial interaction completely. Furthermore, double mutants do not form a stable endothelial monolayer, and display intrajunctional gaps, dislocalization of Zo-1 and defects in apical-basal polarization. In summary, VE-cadherin and Esama have distinct and redundant functions during blood vessel morphogenesis, and both adhesion proteins are central to endothelial cell recognition during anastomosis.