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Polarized actin and VE-cadherin dynamics regulate junctional remodelling and cell migration during sprouting angiogenesis

Author

Listed:
  • Jiahui Cao

    (Westfälische Wilhelms University of Münster, Faculty of Medicine)

  • Manuel Ehling

    (Max Planck Institute for Molecular Biomedicine and Westfälische Wilhelms University of Münster, Faculty of Medicine)

  • Sigrid März

    (Westfälische Wilhelms University of Münster, Faculty of Medicine)

  • Jochen Seebach

    (Westfälische Wilhelms University of Münster, Faculty of Medicine)

  • Katsiaryna Tarbashevich

    (Center for Molecular Biology of Inflammation)

  • Tomas Sixta

    (Czech Technical University)

  • Mara E. Pitulescu

    (Max Planck Institute for Molecular Biomedicine and Westfälische Wilhelms University of Münster, Faculty of Medicine)

  • Ann-Cathrin Werner

    (LMU Munich)

  • Boris Flach

    (Czech Technical University)

  • Eloi Montanez

    (LMU Munich)

  • Erez Raz

    (Center for Molecular Biology of Inflammation)

  • Ralf H. Adams

    (Max Planck Institute for Molecular Biomedicine and Westfälische Wilhelms University of Münster, Faculty of Medicine)

  • Hans Schnittler

    (Westfälische Wilhelms University of Münster, Faculty of Medicine)

Abstract

VEGFR-2/Notch signalling regulates angiogenesis in part by driving the remodelling of endothelial cell junctions and by inducing cell migration. Here, we show that VEGF-induced polarized cell elongation increases cell perimeter and decreases the relative VE-cadherin concentration at junctions, triggering polarized formation of actin-driven junction-associated intermittent lamellipodia (JAIL) under control of the WASP/WAVE/ARP2/3 complex. JAIL allow formation of new VE-cadherin adhesion sites that are critical for cell migration and monolayer integrity. Whereas at the leading edge of the cell, large JAIL drive cell migration with supportive contraction, lateral junctions show small JAIL that allow relative cell movement. VEGFR-2 activation initiates cell elongation through dephosphorylation of junctional myosin light chain II, which leads to a local loss of tension to induce JAIL-mediated junctional remodelling. These events require both microtubules and polarized Rac activity. Together, we propose a model where polarized JAIL formation drives directed cell migration and junctional remodelling during sprouting angiogenesis.

Suggested Citation

  • Jiahui Cao & Manuel Ehling & Sigrid März & Jochen Seebach & Katsiaryna Tarbashevich & Tomas Sixta & Mara E. Pitulescu & Ann-Cathrin Werner & Boris Flach & Eloi Montanez & Erez Raz & Ralf H. Adams & Ha, 2017. "Polarized actin and VE-cadherin dynamics regulate junctional remodelling and cell migration during sprouting angiogenesis," Nature Communications, Nature, vol. 8(1), pages 1-20, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-02373-8
    DOI: 10.1038/s41467-017-02373-8
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    Cited by:

    1. Shinya Yuge & Koichi Nishiyama & Yuichiro Arima & Yasuyuki Hanada & Eri Oguri-Nakamura & Sanshiro Hanada & Tomohiro Ishii & Yuki Wakayama & Urara Hasegawa & Kazuya Tsujita & Ryuji Yokokawa & Takashi M, 2022. "Mechanical loading of intraluminal pressure mediates wound angiogenesis by regulating the TOCA family of F-BAR proteins," Nature Communications, Nature, vol. 13(1), pages 1-25, December.

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