From the 1. Medizinische Klinik und Deutsches Herzzentrum and Institut
für klinische Chemie und Pathobiologie (S.P., D.N., K.B.), Klinikum
rechts der Isar der Technischen Universität München, Germany.
Correspondence to Meinrad Gawaz, MD, 1. Medizinische Klinikum rechts der Isar und Deutsches Herzzentrum, Technische Universität München, Lazarettstraße 36, 80636 München, Germany. E-mail gawaz{at}dhm.mhn.de
Background—Platelet/endothelium
interaction plays an important role in the pathophysiology of
inflammation and atherosclerosis. The role of
platelets for monocyte chemotactic protein-1 (MCP-1) secretion and
surface expression of intercellular adhesion molecule-1 (ICAM-1) on
endothelial cells has been assessed.
Methods and Results—Monolayers of human umbilical vein
endothelial cells were incubated with nonstimulated or
ADP-activated platelets for 6 hours, and secretion of MCP-1
and surface expression of ICAM-1 were determined by ELISA and flow
cytometry, respectively. In the presence of ADP-activated
platelets, both MCP-1 secretion and ICAM-1 surface expression were
significantly increased compared with nonstimulated platelets
(P<0.02). Activation of the transcription factor
nuclear factor-
Conclusions—The present study indicates that
activated platelets modulate chemotactic (MCP-1) and
adhesive (ICAM-1) properties of endothelial cells via
an NF-
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Activated Platelets Induce Monocyte Chemotactic Protein-1 Secretion and Surface Expression of Intercellular Adhesion Molecule-1 on Endothelial Cells
B (NF-B) determined by electrophoretic mobility
shift assay and B-dependent transcriptional activity was enhanced in
the presence of activated platelets. In addition,
ADP-activated platelets induced MCP-1 and ICAM-1
promoter–dependent transcription. Liposomal transfection of a
double-stranded B phosphorothioate oligonucleotide,
but not of the mutated form, inhibited MCP-1 secretion and surface
expression of ICAM-1 on activated endothelium
(P<0.05). B–dependent mechanism. Platelet-induced activation of the
NF-B system might contribute to early inflammatory events in
atherogenesis.
Key Words: platelets • endothelium • proteins • cell adhesion molecules • genes
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