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Published online November 12, 2007
doi:10.1083/jcb.200705002
The Journal of Cell Biology, Vol. 179, No. 4, 761-775
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Furman et al.
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Article

Ena/VASP is required for endothelial barrier function in vivo



Craig Furman1, Alisha L. Sieminski2, Adam V. Kwiatkowski1, Douglas A. Rubinson1, Eliza Vasile1, Roderick T. Bronson3, Reinhard Fässler4, and Frank B. Gertler1

1 Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139
2 Department of Bioengineering, Franklin W. Olin College of Engineering, Needham, MA 02492
3 Department of Pathology, Harvard Medical School, Boston, MA 02115
4 Department for Molecular Medicine, Max Planck Institute for Biochemistry, D-82157 Martinsried, Germany

Correspondence to Frank B. Gertler: fgertler{at}mit.edu

Enabled/vasodilator-stimulated phosphoprotein (Ena/VASP) proteins are key actin regulators that localize at regions of dynamic actin remodeling, including cellular protrusions and cell–cell and cell–matrix junctions. Several studies have suggested that Ena/VASP proteins are involved in the formation and function of cellular junctions. Here, we establish the importance of Ena/VASP in endothelial junctions in vivo by analysis of Ena/VASP-deficient animals. In the absence of Ena/VASP, the vasculature exhibits patterning defects and lacks structural integrity, leading to edema, hemorrhaging, and late stage embryonic lethality. In endothelial cells, we find that Ena/VASP activity is required for normal F-actin content, actomyosin contractility, and proper response to shear stress. These findings demonstrate that Ena/VASP is critical for actin cytoskeleton remodeling events involved in the maintenance of functional endothelia.

C. Furman's present address is Pfizer Research Technology Center, Cambridge, MA 02139.

A.V. Kwiatkowski's present address is Dept. of Biological Sciences, Stanford University, Stanford, CA 94305.

Abbreviations used in this paper: E, embryonic day; Ena/VASP, Enabled/vasodilator-stimulated phosphoprotein; HUVEC, human umbilical vein endothelial cell; Mena, mammalian Ena; MLC, myosin light chain; PECAM, platelet/endothelial cell adhesion molecule; VE-cadherin, vascular endothelial–cadherin; ZO, zonula occludens.


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