The tight junction protein Claudin-5 limits endothelial cell motility.
Adhesive force
Atomic force microscopy
Cell motility
Claudin-5
Dorsal aorta
Vasculogenesis
Journal
Journal of cell science
ISSN: 1477-9137
Titre abrégé: J Cell Sci
Pays: England
ID NLM: 0052457
Informations de publication
Date de publication:
11 01 2021
11 01 2021
Historique:
received:
29
04
2020
accepted:
26
11
2020
pubmed:
17
12
2020
medline:
22
6
2021
entrez:
16
12
2020
Statut:
epublish
Résumé
Steinberg's differential adhesion hypothesis suggests that adhesive mechanisms are important for sorting of cells and tissues during morphogenesis (Steinberg, 2007). During zebrafish vasculogenesis, endothelial cells sort into arterial and venous vessel beds but it is unknown whether this involves adhesive mechanisms. Claudins are tight junction proteins regulating the permeability of epithelial and endothelial tissue barriers. Previously, the roles of claudins during organ development have exclusively been related to their canonical functions in determining paracellular permeability. Here, we use atomic force microscopy to quantify claudin-5-dependent adhesion and find that this strongly contributes to the adhesive forces between arterial endothelial cells. Based on genetic manipulations, we reveal a non-canonical role of Claudin-5a during zebrafish vasculogenesis, which involves the regulation of adhesive forces between adjacent dorsal aortic endothelial cells.
Identifiants
pubmed: 33323504
pii: jcs.248237
doi: 10.1242/jcs.248237
pii:
doi:
Substances chimiques
Claudin-4
0
Claudin-5
0
Claudins
0
Tight Junction Proteins
0
Zebrafish Proteins
0
cldn5a protein, zebrafish
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2021. Published by The Company of Biologists Ltd.
Déclaration de conflit d'intérêts
Competing interestsThe authors declare no competing or financial interests.