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Brain endothelium lack one of two pathways of P-selectin-mediated
neutrophil adhesion
FJ Barkalow, MJ Goodman, ME Gerritsen and TN Mayadas
Department of Pathology, Brigham and Women's Hospital and Harvard Medical
School, Boston, MA 02115, USA.
P-selectin, an endothelial leukocyte adhesion receptor, is rapidly
translocated to the cell surface upon release from storage granules called
Weibel-Palade bodies and is also transcriptionally upregulated upon
cytokine stimulation of endothelial cells (ECs). These two pathways of
surface expression are coincident with the rapid and cytokine-inducible
pathway of neutrophil adhesion to ECs. Constitutive P-selectin expression
is largely absent in cultured murine brain microvascular EC (BMEC)
monolayers, but interleukin-1beta and tumor necrosis factor-alpha
stimulation for 4 hours leads to dramatic P- selectin upregulation. The
functional relevance of differential P- selectin expression in these cells
was examined by studying BMECs derived from wild-type mice and
P-selectin-deficient mice. We show that P-selectin deficiency does not
affect Weibel-Palade body formation or their release in response to
short-acting agonists. However, in the absence of P-selectin, the brain
endothelium is unable to support neutrophil adhesion after stimulation with
these agonists, which may contribute to the immune privilege status of the
brain. We show that P- selectin does play a major role in supporting
neutrophil adhesion in the cytokine-induced pathway in BMECs in the context
of other cytokine- inducible endothelial-leukocyte adhesion receptors,
E-selectin, ICAM-1, and VCAM-1.
Volume 88,
Issue 12,
pp. 4585-4593,
12/15/1996
Copyright © 1996 by The American Society of Hematology
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