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Wnt/β-catenin signaling regulates VE-cadherin-mediated anastomosis of brain capillaries by counteracting S1pr1 signaling

Author

Listed:
  • Kathleen Hübner

    (University of Muenster
    Cells-in-Motion Cluster of Excellence (EXC 1003 – CiM), University of Muenster)

  • Pauline Cabochette

    (Université libre de Bruxelles)

  • Rodrigo Diéguez-Hurtado

    (Cells-in-Motion Cluster of Excellence (EXC 1003 – CiM), University of Muenster
    Max Planck Institute for Molecular Biomedicine)

  • Cora Wiesner

    (Biozentrum der Universität Basel)

  • Yuki Wakayama

    (University of Muenster)

  • Kathrin S. Grassme

    (University of Muenster)

  • Marvin Hubert

    (University of Muenster)

  • Stefan Guenther

    (Max Planck Institute for Heart and Lung Research, ECCPS Bioinformatics and Deep Sequencing Platform)

  • Heinz-Georg Belting

    (Biozentrum der Universität Basel)

  • Markus Affolter

    (Biozentrum der Universität Basel)

  • Ralf H. Adams

    (Cells-in-Motion Cluster of Excellence (EXC 1003 – CiM), University of Muenster
    Max Planck Institute for Molecular Biomedicine)

  • Benoit Vanhollebeke

    (Université libre de Bruxelles
    Walloon Excellence in Life Sciences and Biotechnology (WELBIO))

  • Wiebke Herzog

    (University of Muenster
    Cells-in-Motion Cluster of Excellence (EXC 1003 – CiM), University of Muenster
    Max Planck Institute for Molecular Biomedicine)

Abstract

Canonical Wnt signaling is crucial for vascularization of the central nervous system and blood-brain barrier (BBB) formation. BBB formation and modulation are not only important for development, but also relevant for vascular and neurodegenerative diseases. However, there is little understanding of how Wnt signaling contributes to brain angiogenesis and BBB formation. Here we show, using high resolution in vivo imaging and temporal and spatial manipulation of Wnt signaling, different requirements for Wnt signaling during brain angiogenesis and BBB formation. In the absence of Wnt signaling, premature Sphingosine-1-phosphate receptor (S1pr) signaling reduces VE-cadherin and Esama at cell-cell junctions. We suggest that Wnt signaling suppresses S1pr signaling during angiogenesis to enable the dynamic junction formation during anastomosis, whereas later S1pr signaling regulates BBB maturation and VE-cadherin stabilization. Our data provides a link between brain angiogenesis and BBB formation and identifies Wnt signaling as coordinator of the timing and as regulator of anastomosis.

Suggested Citation

  • Kathleen Hübner & Pauline Cabochette & Rodrigo Diéguez-Hurtado & Cora Wiesner & Yuki Wakayama & Kathrin S. Grassme & Marvin Hubert & Stefan Guenther & Heinz-Georg Belting & Markus Affolter & Ralf H. A, 2018. "Wnt/β-catenin signaling regulates VE-cadherin-mediated anastomosis of brain capillaries by counteracting S1pr1 signaling," Nature Communications, Nature, vol. 9(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07302-x
    DOI: 10.1038/s41467-018-07302-x
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