A1 Refereed original research article in a scientific journal
Junction-based lamellipodia drive endothelial cell rearrangements in vivo via a VE-cadherin-F-actin based oscillatory cell-cell interaction
Authors: Ilkka Paatero, Loïc Sauteur, Minkyoung Lee, Anne K. Lagendijk, Daniel Heutschi, Cora Wiesner, Camilo Guzmán, Dimitri Bieli, Benjamin M. Hogan, Markus Affolter, Heinz-Georg Belting
Publisher: NATURE PUBLISHING GROUP
Publication year: 2018
Journal: Nature Communications
Journal name in source: NATURE COMMUNICATIONS
Journal acronym: NAT COMMUN
Article number: 3545
Volume: 9
First page : 1
Last page: 13
Number of pages: 13
ISSN: 2041-1723
DOI: https://doi.org/10.1038/s41467-018-05851-9
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/35817952
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.
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