期刊
DEVELOPMENT
卷 144, 期 8, 页码 1554-1565出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.140038
关键词
Angiogenesis; Anastomosis; Cell contact formation; Morphogenesis; Cell adhesion; Esam; VE-cadherin; Cdh5; Endothelial cell; Zebrafish
资金
- Werner Siemens-Stiftung
- Basel-Stadt
- Basel-Land Kantons
- Schweizerischer Nationalfonds zur Forderung der Wissenschaftlichen Forschung [156838]
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.
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