Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:2286-2297
© 1999 American Heart Association, Inc.
Vascular Biology |
Histamine Induces Tyrosine Phosphorylation of Endothelial Cell-to-Cell Adherens Junctions
Abstract—Endothelial adherens junctions (AJ) promote intercellular adhesion and may contribute to the control of vascular permeability. These structures are formed by a transmembrane and cell-specific adhesive protein, vascular endothelial (VE)-cadherin, which is linked by its cytoplasmic tail to intracellular proteins called catenins (
-catenin, ß-catenin, and plakoglobin) and to the actin
cytoskeleton. Little is known about the functional regulation of AJ in
endothelial cells. In this study, we analyzed
the effect of histamine on AJ organization in cultured
endothelial cells. We first observed that histamine
induced detectable intercellular gaps only in loosely-confluent cells,
whereas this effect was strongly reduced or absent in long-confluent
cultures. Despite this difference, in vitro permeability was augmented
by histamine in both conditions. In resting conditions, tyrosine
phosphorylation of AJ components and permeability
values were higher in recently-confluent cells as compared with
long-confluent cells. Histamine did not affect the
phosphorylation state of AJ in recently-confluent cells
but strongly increased this parameter in long-confluent
cultures. In addition, in long-confluent cells, histamine caused
dissociation of VE-cadherin from the actin cytoskeleton measured by a
decrease of the amount of the molecule in the detergent-insoluble
fraction of the cell extracts. Dibutyryl cAMP was able to prevent the
effect of histamine on both tyrosine phosphorylation of
AJ components and on endothelial permeability. The
effect of histamine was specific for VE-cadherin because the
phosphorylation state of neural (N)-cadherin,
the other major endothelial cadherin, was unchanged by
this agent. Hence AJ components are a target of histamine activation
cascade; we suggest that induction of tyrosine
phosphorylation of VE-cadherin and catenins contributes
to the histamine effect on permeability, even in absence of frank
intercellular gaps and cell retraction.
Key Words: endothelial cells • inflammatory mediators • adhesion molecules • cell-to-cell interactions
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