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AmotL2 links VE-cadherin to contractile actin fibres necessary for aortic lumen expansion.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Hematology and Immunology.
2014 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 5, 3743Article in journal (Refereed) Published
Abstract [en]

The assembly of individual endothelial cells into multicellular tubes is a complex morphogenetic event in vascular development. Extracellular matrix cues and cell-cell junctional communication are fundamental to tube formation. Together they determine the shape of endothelial cells and the tubular structures that they ultimately form. Little is known regarding how mechanical signals are transmitted between cells to control cell shape changes during morphogenesis. Here we provide evidence that the scaffold protein amotL2 is needed for aortic vessel lumen expansion. Using gene inactivation strategies in zebrafish, mouse and endothelial cell culture systems, we show that amotL2 associates to the VE-cadherin adhesion complex where it couples adherens junctions to contractile actin fibres. Inactivation of amotL2 dissociates VE-cadherin from cytoskeletal tensile forces that affect endothelial cell shape. We propose that the VE-cadherin/amotL2 complex is responsible for transmitting mechanical force between endothelial cells for the coordination of cellular morphogenesis consistent with aortic lumen expansion and function.

Place, publisher, year, edition, pages
2014. Vol. 5, 3743
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-279314DOI: 10.1038/ncomms4743OAI: oai:DiVA.org:uu-279314DiVA: diva2:907829
Available from: 2016-02-29 Created: 2016-02-29 Last updated: 2016-02-29

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Publisher's full texthttp://www.nature.com/ncomms/2014/140507/ncomms4743/full/ncomms4743.html
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