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

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 and Hans Schnittler ()
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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

Nature Communications, 2017, vol. 8, issue 1, 1-20

Abstract: 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.

Date: 2017
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DOI: 10.1038/s41467-017-02373-8

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