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J Biol Chem, Vol. 274, Issue 50, 35562-35570, December 10, 1999
From the Departments of The eicosanoid thromboxane
A2 (TXA2) is released by activated
platelets, monocytes, and the vessel wall and interacts with high
affinity receptors expressed in several tissues including endothelium.
Whether TXA2 might alter endothelial migration and tube
formation, two determinants of angiogenesis, is unknown. Thus, we
investigated the effect of the TXA2 mimetic
[1S-(1
Inhibition of Endothelial Cell Migration, Intercellular
Communication, and Vascular Tube Formation by Thromboxane
A2*
§,,
,**,, and
Medicine (Cardiology),
Molecular Pharmacology, ¶ Pathology,
and Neuroscience, the Albert Einstein College of Medicine of
Yeshiva University, Bronx, New York 10461 and the ** University Sao
Judas Tadeu, Sao Paulo 03166-000, Brazil
,2
(5Z),3(1E,3R),4]-7-[3-(3-hydroxy-4-(4'-iodophenoxy)-1-butenyl)-7-oxabicyclo-[2.2.1]heptan-2-yl]-5'-heptenoic acid (IBOP) on human endothelial cell (HEC) migration and
angiogenesis in vitro. IBOP stimulation inhibited HEC
migration by 50% and in vitro capillary formation by 75%.
These effects of IBOP were time- and
concentration-dependent with an IC50 of 25 nM. IBOP did not affect integrin expression or cytoskeletal
morphology of HEC. Since gap junction-mediated intercellular
communication increases in migrating HEC, we determined whether IBOP
might inhibit coupling or connexin expression in HEC. IBOP reduced the
passage of microinjected dyes between HEC by 50%, and the effects of
IBOP on migration and tube formation were mimicked by the gap junction inhibitor 18-glycyrrhetinic acid (1 µM) with a similar
time course and efficacy. IBOP (24 h) did not affect the expression or
phosphorylation of connexin 43 in whole HEC lysates. Immunohistologic
examination of HEC suggested that IBOP may impair functional coupling
by altering the cellular distribution of gap junctions, leading to
increased connexin 43 internalization. Thus, this finding that
TXA2 mimetics can prevent HEC migration and tube formation,
possibly by impairing intercellular communication, suggests that
antagonizing TXA2 signaling might enhance vascularization
of ischemic tissue.
*
This work was supported by National Institutes of Health
Grants HL47032-05 and HL38449 and Fundacao de Amparo a Pesquisa do Estado de Sao Paulo, Brazil, Grant J997/2379-2.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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