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Vol. 281, Issue 2, 655-662, 1997
Department of Medicine, Division of Clinical Immunology, Johns
Hopkins University School of Medicine, Baltimore, Maryland
Cysteinyl leukotrienes are bioactive lipid mediators known to possess
potent proinflammatory actions. Included in these are effects on
vascular endothelium to promote surface expression of the adhesion
molecule P-selectin. In the present study we were interested in
investigating the receptor mechanism(s) involved in cysteinyl
leukotriene-induced endothelial P-selectin expression. As such we
examined the effect of several potent and selective cysteinyl
leukotriene receptor antagonists on this response. Incubation of
cultured human umbilical vein endothelial cells (HUVEC) with the
cysteinyl leukotrienes leukotriene C4 (LTC4) or
leukotriene D4 (LTD4) induced surface
expression of P-selectin which was concentration dependent and rapid in
onset. Expression of endothelial P-selectin induced by either
LTC4 or LTD4 was not blocked however by
pretreatment of HUVEC with the selective cysteinyl leukotriene-1
(CysLT1) receptor antagonists SKF 104353, pranlukast or zafirlukast before agonist exposure. In contrast, SKF
104353 effectively antagonized the LTC4-induced
contractions in isolated human bronchial smooth muscle preparations,
shifting the agonist dose-response curve to the right by some 3 log-fold in this tissue. The present results suggest that cysteinyl
leukotrienes induce surface expression of endothelial P-selectin
via a mechanism independent of the
CysLT1 receptor.
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