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.
Date: 2017
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
MeSH Terms:
  • Animals
  • Antigens, CD/metabolism*
  • Blood Vessels/embryology*
  • Blood Vessels/metabolism*
  • Cadherins/metabolism*
  • Cell Adhesion Molecules/metabolism*
  • Cell Communication
  • Cell Polarity
  • Endothelial Cells/cytology
  • Endothelial Cells/metabolism
  • Intercellular Junctions/metabolism
  • Morphogenesis*
  • Mutation/genetics
  • Neovascularization, Physiologic*
  • Pseudopodia/metabolism
  • Zebrafish/embryology*
  • Zebrafish/metabolism*
  • Zebrafish Proteins/metabolism*
PubMed: 28264837 Full text @ Development
The 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.