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Cdh5/VE-cadherin promotes endothelial cell interface elongation via cortical actin polymerization during angiogenic sprouting.
Journal article

Cdh5/VE-cadherin promotes endothelial cell interface elongation via cortical actin polymerization during angiogenic sprouting.

  • Sauteur L Biozentrum der Universität Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland.
  • Krudewig A Biozentrum der Universität Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland.
  • Herwig L Biozentrum der Universität Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland.
  • Ehrenfeuchter N Biozentrum der Universität Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland.
  • Lenard A Biozentrum der Universität Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland.
  • Affolter M Biozentrum der Universität Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland. Electronic address: markus.affolter@unibas.ch.
  • Belting HG Biozentrum der Universität Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland. Electronic address: heinz-georg.belting@unibas.ch.
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  • 2014-11-07
Published in:
  • Cell reports. - 2014
Actin Cytoskeleton
Actins
Animals
Antigens, CD
Cadherins
Cell Movement
Endothelial Cells
Endothelium, Vascular
Intercellular Junctions
Myosins
Neovascularization, Physiologic
Polymerization
Zebrafish
English Organ morphogenesis requires the coordination of cell behaviors. Here, we have analyzed dynamic endothelial cell behaviors underlying sprouting angiogenesis in vivo. Two different mechanisms contribute to sprout outgrowth: tip cells show strong migratory behavior, whereas extension of the stalk is dependent upon cell elongation. To investigate the function of Cdh5 in sprout outgrowth, we generated null mutations in the zebrafish cdh5 gene, and we found that junctional remodeling and cell elongation are impaired in mutant embryos. The defects are associated with a disorganization of the actin cytoskeleton and cannot be rescued by expression of a truncated version of Cdh5. Finally, the defects in junctional remodeling can be phenocopied by pharmacological inhibition of actin polymerization, but not by inhibiting actin-myosin contractility. Taken together, our results support a model in which Cdh5 organizes junctional and cortical actin cytoskeletons, as well as provides structural support for polymerizing F-actin cables during endothelial cell elongation.
Language
  • English
Open access status
gold
Identifiers
Persistent URL
https://sonar.ch/global/documents/232068
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