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Localization of 13-hydroxyoctadecadienoic acid and the vitronectin receptor
in human endothelial cells and endothelial cell/platelet interactions in
vitro
MR Buchanan, MC Bertomeu, TA Haas, FW Orr and LL Eltringham-Smith
Department of Pathology, McMaster University, Hamilton, Ontario, Canada.
Blood/vessel wall cell interactions depend, in part, on the expression of
adhesion receptors on cell surfaces, such as expression of the vitronectin
receptor (VnR) on the apical surface of endothelial cells (ECs) for
platelet/EC adhesion. However, it is unclear how receptor expression is
regulated from within cells. In previous studies, we found that ECs
metabolize linoleic acid into the lipoxygenase monohydroxide,
13-hydroxyoctadecadienoic acid (13-HODE), and that the intracellular level
of 13-HODE correlates inversely with VnR expression and platelet adhesion
to the EC apical surface. In this study, we determined the physical
associations of 13-HODE and VnR in unstimulated and stimulated ECs, ie, at
times when ECs were and were not adhesive for specific ligands and
platelets, using double antibody immunofluorescent staining techniques and
binding assays. 13-HODE and the VnR were colocalized within unstimulated
ECs. When ECs were stimulated, 13-HODE was no longer detectable, either in
or outside the ECs, and the VnR was detected on the apical surface of the
ECs. These changes were paralleled by increased vitronectin binding and
increased platelet adhesion to the ECs. We suggest that colocalization of
13-HODE with VnR reflects a 13-HODE/VnR interaction, confining the VnR in a
nonadhesive form inside unstimulated ECs, and, as a result, the ECs are
nonadhesive. When the ECs are stimulated, 13-HODE and VnR dissociate,
allowing the VnR to relocate on the EC surface, where the VnR undergoes a
conformational change resulting in increased EC adhesivity.
Volume 81,
Issue 12,
pp. 3303-3312,
06/15/1993
Copyright © 1993 by The American Society of Hematology
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