The tight junctions protein Claudin-5 limits endothelial cell motility
- Yang, Z., Wu, S., Fontana, F., Li, Y., Xiao, W., Gao, Z., Stephan, A., Affolter, M., Belting, H.G., Abdelilah-Seyfried, S., Zhang, J.
- Journal of Cell Science 134(1): (Journal)
- Registered Authors
- Abdelilah-Seyfried, Salim, Affolter, Markus, Belting, Heinz-Georg Paul (Henry), Zhang, Jingjing
- Adhesive force, Atomic force microscopy, Cell motility, Claudin-5, Dorsal aorta, Vasculogenesis
- MeSH Terms
- Endothelial Cells
- Tight Junction Proteins*
- Tight Junctions*
- 33323504 Full text @ J. Cell Sci.
Yang, Z., Wu, S., Fontana, F., Li, Y., Xiao, W., Gao, Z., Stephan, A., Affolter, M., Belting, H.G., Abdelilah-Seyfried, S., Zhang, J. (2020) The tight junctions protein Claudin-5 limits endothelial cell motility. Journal of Cell Science. 134(1):.
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. In vitro and in vivo studies demonstrate that loss of Claudin-5 results in increased motility of dorsal aorta endothelial cells and in a failure of the dorsal aorta to lumenize. Our findings uncover a novel role of Claudin-5 in limiting arterial endothelial cell motility, which goes beyond its traditional sealing function during embryonic development.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes