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© The Rockefeller University Press, 0021-9525/2000//203 $5.00
The Journal of Cell Biology, Volume 148, Number 1, , 2000 203-216

Original Article

Monocytes Induce Reversible Focal Changes in Vascular Endothelial Cadherin Complex during Transendothelial Migration under Flow



Jennifer R. Allporta, William A. Mullerb, and Francis W. Luscinskasa

a Vascular Research Division, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115
b Department of Pathology, Weill Medical College of Cornell University, New York, New York 10021
Department of Pathology, Brigham and Women's Hospital, 221 Longwood Avenue, Boston, MA 02115.(617) 732-5933(617) 732-6004

fluscinskas{at}rics.bwh.harvard.edu

The vascular endothelial cell cadherin complex (VE-cadherin, {alpha}-, β-, and {gamma}-catenin, and p120/p100) localizes to adherens junctions surrounding vascular endothelial cells and may play a critical role in the transendothelial migration of circulating blood leukocytes. Previously, we have reported that neutrophil adhesion to human umbilical vein endothelial cell (HUVEC) monolayers, under static conditions, results in a dramatic loss of the VE-cadherin complex. Subsequent studies by us and others (Moll, T., E. Dejana, and D. Vestweber. 1998. J. Cell Biol. 140:403–407) suggested that this phenomenon might reflect degradation by neutrophil proteases released during specimen preparation. We postulated that some form of disruption of the VE-cadherin complex might, nonetheless, be a physiological process during leukocyte transmigration. In the present study, the findings demonstrate a specific, localized effect of migrating leukocytes on the VE-cadherin complex in cytokine-activated HUVEC monolayers. Monocytes and in vitro differentiated U937 cells induce focal loss in the staining of VE-cadherin, {alpha}-catenin, β-catenin, and plakoglobin during transendothelial migration under physiological flow conditions. These events are inhibited by antibodies that prevent transendothelial migration and are reversed following transmigration. Together, these data suggest that an endothelial-dependent step of transient and focal disruption of the VE-cadherin complex occurs during leukocyte transmigration.

Key Words: adherens junctions • catenins • adhesion molecules • cell-to-cell interactions • recruitment

© 2000 The Rockefeller University Press

Abbreviations used in this paper: [Ca2+]i, intracellular Ca2+ concentration; DPBS, Dulbecco's phosphate-buffered saline; HSA, human serum albumin; HUVEC, human umbilical vein endothelial cells; ICAM-1, intercellular adhesion molecule 1; PBMC, peripheral blood mononuclear cells; PECAM-1, platelet endothelial cell adhesion molecule 1; PMN, polymorphonuclear leukocytes; TNF-{alpha}, tumor necrosis factor {alpha}; U937L, U937 monocytic cells stably transfected with L-selectin (CD62L); U937L-Dif, differentiated U937L; VE-cadherin, vascular endothelial cell cadherin.


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