4.5 Article

The tight junction protein Claudin-5 limits endothelial cell motility

期刊

JOURNAL OF CELL SCIENCE
卷 134, 期 1, 页码 -

出版社

COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.248237

关键词

Claudin-5; Adhesive force; Dorsal aorta; Atomic force microscopy; Vasculogenesis; Cell motility

资金

  1. National Key Research and Development Program of China [2018YFA0801200, 2018YFA0801000]
  2. National Natural Science Foundation of China [31970777, 31771628, 31370824]
  3. Guangdong Natural Science Fund for Distinguished Young Scholars [2017A030306024]
  4. Deutsche Forschungsgemeinschaft (DFG) [SFB958, SE2016/7-2, SE2016/10-1, SE2016/13-1]

向作者/读者索取更多资源

The research reveals a non-canonical role of claudin-5 in zebrafish vasculogenesis, where it regulates adhesive forces between arterial endothelial cells, limiting cell motility and affecting lumen formation in the artery.
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 increasedmotility 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.

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