(Circulation. 1997;96:1809-1818.)
© 1997 American Heart Association, Inc.
Articles |
Vitronectin Receptor (
vß3) Mediates Platelet Adhesion to the Luminal Aspect of Endothelial Cells
Implications for Reperfusion in Acute Myocardial Infarction
From the 1. Medizinische Klinik der Technischen Universität München, Germany.
Correspondence to Dr Meinrad Gawaz, 1. Medizinische Klinik der Technischen Universität München, Klinikum rechts der Isar, Ismaninger Straße 22, 81675 München, Germany.
Background Platelet interaction with
endothelium plays an important role in the
pathophysiology of coronary microcirculation. We assessed the
role of the vitronectin receptor (integrin
vß3) in
platelet/endothelium adhesion.
Methods and Results We investigated the effect on
platelet/endothelium adhesion of plasma obtained
from patients with acute myocardial infarction during reperfusion
(before and 8, 24, 48, and 72 hours and 5 to 7 days after direct
angioplasty) and with pretreatment with -thrombin (2 U/mL) and
recombinant human interleukin-1ß.
Platelet/endothelium adhesion was significantly
enhanced by 
20% after pretreatment of endothelium
with patient plasma for 4 hours (P<.05) compared with
endothelium treated with pooled control plasma.
Plasma-induced platelet/endothelium adhesion was,
in part, RGD peptide dependent. Pretreatment of
endothelial cells with -thrombin or recombinant
human interleukin-1ß enhanced
platelet/endothelium adhesion and surface
expression of vß3 on the luminal aspect of
endothelium (P<.05). The adhesion of
platelets, isolated platelet microparticles, and Chinese
hamster ovary cells bearing human recombinant
IIbß3 (platelet
glycoprotein IIb-IIIa) to activated
endothelial cells was inhibited by antiadhesive
peptides GRGDSP and c(RGDfV) and monoclonal antibodies 4F10, LM609, and
7E3.
Conclusions The expression of vitronectin receptor exposed on the luminal aspect of activated endothelium is enhanced and mediates platelet/endothelium adhesion. Vitronectin receptor–mediated platelet attachment to activated endothelium during reperfusion may contribute to reperfusion injury and could be a target for antiadhesive therapy.
Key Words: platelets • endothelium • myocardial infarction • reperfusion • integrins
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