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Fluid shear stress modulates surface expression of adhesion molecules by
endothelial cells
M Morigi, C Zoja, M Figliuzzi, M Foppolo, G Micheletti, M Bontempelli, M Saronni, G Remuzzi and A Remuzzi
Mario Negri Institute for Pharmacological Research, Bergamo, Italy.
We investigated the effect of hemodynamic shear forces on the expression of
adhesive molecules, E-selectin, and intercellular adhesion molecule-1
(ICAM-1) on human umbilical vein endothelial cells (HUVEC) exposed to
laminar (8 dynes/cm2) or turbulent shear stress (8.6 dynes/cm2 average), or
to a static condition. Laminar flow induced a significant time-dependent
increase in the surface expression of ICAM- 1, as documented by flow
cytometry studies. Endothelial cell surface expression of ICAM-1 in
supernatants of HUVEC exposed to laminar flow was not modified, excluding
the possibility that HUVEC exposed to laminar flow synthetize factors that
upregulate ICAM-1. The effect of laminar flow was specific for ICAM-1,
while E-selectin expression was not modulated by the flow condition.
Turbulent flow did not affect surface expression of either E-selectin or
ICAM-1. To evaluate the functional significance of the laminar-flow-induced
increase in ICAM-1 expression, we studied the dynamic interaction of total
leukocyte suspension with HUVEC exposed to laminar flow (8 dynes/cm2 for 6
hours) in a parallel-plate flow chamber or to static condition. Leukocyte
adhesion to HUVEC pre-exposed to flow was significantly enhanced, compared
with HUVEC maintained in static condition (233 +/- 67 v 43 +/- 16
leukocytes/mm2, respectively), and comparable with that of interleukin-1
beta treated HUVEC. Mouse monoclonal antibody anti-ICAM-1 completely
blocked flow-induced upregulation of leukocyte adhesion. Interleukin-1
beta, which upregulated E-selectin expression, caused leukocyte rolling on
HUVEC that was significantly lower on flow- conditioned HUVEC and almost
absent on untreated static endothelial cells. Thus, laminar flow directly
and selectively upregulates ICAM-1 expression on the surface of endothelial
cells and promotes leukocyte adhesion. These data are relevant to the
current understanding of basic mechanisms that govern local inflammatory
reactions and tissue injury.
Volume 85,
Issue 7,
pp. 1696-1703,
04/01/1995
Copyright © 1995 by The American Society of Hematology
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