Junction-based lamellipodia drive endothelial cell rearrangements in vivo via a VE-cadherin-F-actin based oscillatory cell-cell interaction

Ilkka Paatero, Loïc Sauteur, Minkyoung Lee, Anne K. Lagendijk, Daniel Heutschi, Cora Wiesner, Camilo Guzmán, Dimitri Bieli, Benjamin M. Hogan, Markus Affolter () and Heinz-Georg Belting ()
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Ilkka Paatero: University of Basel
Loïc Sauteur: University of Basel
Minkyoung Lee: University of Basel
Anne K. Lagendijk: The University of Queensland
Daniel Heutschi: University of Basel
Cora Wiesner: University of Basel
Camilo Guzmán: The University of Queensland
Dimitri Bieli: University of Basel
Benjamin M. Hogan: The University of Queensland
Markus Affolter: University of Basel
Heinz-Georg Belting: University of Basel

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract Angiogenesis and vascular remodeling are driven by extensive endothelial cell movements. Here, we present in vivo evidence that endothelial cell movements are associated with oscillating lamellipodia-like structures, which emerge from cell junctions in the direction of cell movements. High-resolution time-lapse imaging of these junction-based lamellipodia (JBL) shows dynamic and distinct deployment of junctional proteins, such as F-actin, VE-cadherin and ZO1, during JBL oscillations. Upon initiation, F-actin and VE-cadherin are broadly distributed within JBL, whereas ZO1 remains at cell junctions. Subsequently, a new junction is formed at the front of the JBL, which then merges with the proximal junction. Rac1 inhibition interferes with JBL oscillations and disrupts cell elongation—similar to a truncation in ve-cadherin preventing VE-cad/F-actin interaction. Taken together, our observations suggest an oscillating ratchet-like mechanism, which is used by endothelial cells to move over each other and thus provides the physical means for cell rearrangements.

Date: 2018
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DOI: 10.1038/s41467-018-05851-9

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