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Vol. 300, Issue 3, 729-735, March 2002
CarePoint Diagnostics, Inc., Eden Prairie, Minnesota (R.J.S.); and
Pfizer Global Research, Ann Arbor Laboratories, Ann Arbor, Michigan
(K.S.K.)
The role of inflammation in cardiovascular disease and especially in
thrombogenesis has become increasingly recognized as an important
component of the overall disease process. Plaque rupture promotes
activation of the inflammatory response and increased expression of
tissue factor (TF), which in turn acts as one of the major initiators
of extrinsic coagulation. It is becoming apparent that the expression
of TF on endothelial cells, underlying smooth muscle cells and
monocytes is regulated, in part, by proinflammatory cytokines including
tumor necrosis factor and IL-1. In addition to initiating
coagulation, interaction of TF with the adhesion molecule, P-selectin,
has been demonstrated to accelerate the rate and extent of fibrin
formation and deposition. P-selectin is expressed on activated
platelets and endothelium and serves as the receptor for the endogenous
ligand, P-selectin glycoprotein-1 (PSGL-1), expressed on various
leukocytic cell types. In addition to mediating transient interactions
between endothelial cells and leukocytes, P-selectin has been reported
to mediate adherence of platelets to monocytes and neutrophils via
specific interaction with PSGL-1. P-selectin is rapidly cleaved off the
surface of the platelet membrane and appears in the circulation as a
soluble form, which has been reported to be elevated in patients with acute coronary syndromes including unstable angina and non-Q-wave myocardial infarction. This review will focus on the role of cytokines in mediating TF expression and also explore the significance of the
relationship between P-selectin and tissue factor in thrombus generation. In addition, possible pharmacological mechanisms to interrupt this disease process will be discussed.
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