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Blood, Vol. 92 No. 9 (November 1), 1998:
pp. 3445-3454
Enhanced Adherence of Sickle Erythrocytes to Thrombin-Treated
Endothelial Cells Involves Interendothelial Cell Gap Formation
Annamaria B. Manodori,
Neil M. Matsui,
James Y. Chen, and
Stephen
H. Embury
From the Hematology Division, the Department of Medicine, The
University of California-San Francisco and The San Francisco General
Hospital, San Francisco; and the Northern California Comprehensive
Sickle Cell Center, San Francisco, CA.
The adherence of sickle erythrocytes to vascular endothelium has the
capacity to initiate vasoocclusion. The known effects of thrombin on
endothelial cell function and the increased activity of thrombin in
sickle cell disease led us to examine the effect of thrombin on the
adhesivity of cultured endothelial cells for sickle erythrocytes. In
particular, we studied whether the effect of thrombin on
interendothelial cell gap formation (ICGF) was involved in endothelial
cell adhesivity for sickle erythrocytes. Those endothelial cell
monolayers stimulated by thrombin to maximal levels of static sickle
erythrocyte adherence also underwent striking cell contraction and
enlargement of interendothelial cell gaps. Adhesivity also increased
when gaps were induced with antilaminin antibodies or EDTA. Maximally
adhesogenic thrombin conditions failed to increase adhesivity when gap
formation was prevented by pretreatment of the monolayers with
8-bromo-cyclic adenosine monophosphate (bromo-cAMP) or
glutaraldehyde, agents that respectively inhibit
actin-myosin-dependent cell contraction or cross-link adjacent cells
in the monolayer. The influence of these two agents on EDTA-enhanced
adhesivity was linked to their ability to prevent gap formation.
Glutaraldehyde prevented both increased adherence and gap formation;
bromo-cAMP prevented neither. Interendothelial cell gap formation may
contribute to vasoocclusion by facilitating sickle erythrocyte
adherence.
© 1998 by The American Society of Hematology.
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