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Blood, Vol. 92 No. 9 (November 1), 1998:
pp. 3064-3072
Endothelin-1 Induces Production of the Neutrophil Chemotactic Factor
Interleukin-8 by Human Brain-Derived Endothelial Cells
F.M. Hofman,
P. Chen,
R. Jeyaseelan,
F. Incardona,
M. Fisher, and
R. Zidovetzki
From the Departments of Pathology, Medicine, and Neurology,
University of Southern California, Los Angeles; and the Departments of
Biology and Neuroscience, University of California, Riverside, CA.
Increased levels of endothelin-1 (Et-1), a potent vasoconstrictor,
have been correlated with hypertension and neuronal damage in
ischemic/reperfusion injury. The presence of polymorphonuclear cells
(PMNs) in the brain has been shown to be directly responsible for this
observed pathology. To address the question of whether Et-1 plays a
role in this process, human brain-derived endothelial cells (CNS-ECs)
were cultured with Et-1. The results demonstrate that Et-1 induces
production of the neutrophil chemoattractant interleukin-8 (IL-8)
twofold to threefold after 72 hours; mRNA was maximal after 1 hour of
stimulation. Conditioned culture medium derived from Et-1-stimulated
CNS-ECs induced a chemotactic response in the PMN migration assay. The
inflammatory cytokines tumor necrosis factor- (TNF) and IL-1
functioned additively with Et-1 in increasing IL-8 production. In
contrast, transforming growth factor- (TGF-), but not IL-10,
completely abolished the effect of Et-1 on IL-8 production. However,
Et-1 did not modulate intercellular adhesion molecule-1 (ICAM-1)
expression. These data demonstrate that Et-1 may be a risk factor in
ischemic/reperfusion injury by inducing increased levels of the
neutrophil chemoattractant IL-8.
© 1998 by The American Society of Hematology.
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