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Blood, Vol. 95 No. 10 (May 15), 2000:
pp. 3232-3241
Perfusion with sickle erythrocytes up-regulates ICAM-1 and
VCAM-1 gene expression in cultured human
endothelial cells
Yan-Ting Shiu,
Mark M. Udden, and
Larry V. McIntire
From the Cox Laboratory for Biomedical Engineering, Rice University,
and the Department of Medicine, Baylor College of Medicine, Houston,
TX.
Sickle cell anemia is characterized by periodic vasoocclusive
crises. Increased adhesion of sickle erythrocytes to vascular endothelium is a possible contributing factor to vasoocclusion. This
study determined the effect of sickle erythrocyte perfusion at a venous
shear stress level (1 dyne/cm2) on endothelial cell (EC)
monolayers. Sickle erythrocytes up-regulated intercellular adhesion
molecule-1 (ICAM-1) gene expression in cultured human
endothelial cells. This was accompanied by increased cell surface
expression of ICAM-1 and also elevated release of soluble
ICAM-1 molecules. Expression of vascular cell adhesion molecule-1
(VCAM-1) messenger RNA (mRNA) was also strikingly elevated in cultured
ECs after exposure to sickle cell perfusion, although increases in
membrane-bound and soluble VCAM-1 levels were small. The presence of
cytokine interleukin-1 in the perfusion system enhanced the
production of ICAM-1 and VCAM-1 mRNA, cell surface expression, and the
concentrations of circulating forms. This is the first demonstration
that sickle erythrocytes have direct effects on gene regulation in
cultured human ECs under well-defined flow environments. The results
suggest that perfusion with sickle erythrocytes increases the
expression of cell adhesion molecules on ECs and stimulates the release
of soluble cell adhesion molecules, which may serve as indicators of
injury and/or activation of endothelial cells. The interactions between
sickle red blood flow, inflammatory cytokines, and vascular adhesion
events may render sickle cell disease patients vulnerable to
vasoocclusive crises.
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