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Blood, Vol. 92 No. 10 (November 15), 1998:
pp. 3924-3935
Interaction of Sickle Erythrocytes With Endothelial Cells in the
Presence of Endothelial Cell Conditioned Medium Induces Oxidant Stress
Leading to Transendothelial Migration of Monocytes
Chand Sultana,
Yamin Shen,
Vinod Rattan,
Cage Johnson, and
Vijay
K. Kalra
From the Departments of Biochemistry and Molecular Biology, and
Medicine, University of Southern California, School of Medicine, Los
Angeles, CA.
The abnormal adherence of sickle red blood cells (SS RBC) to
endothelial cells has been thought to contribute to vascular occlusion,
a major cause of morbidity in sickle cell disease (SCD). We determined
whether the interaction of SS RBC with cultured endothelial cells
induced cellular oxidant stress that would culminate in expression of
cell adhesion molecules (CAMs) involved in the adhesion and diapedesis
of monocytes and the adherence of SS reticulocytes. We showed that the
interaction of SS RBC at 2% concentration in the presence of multimers
of von Willebrand factor (vWf), derived from endothelial cell-derived
conditioned medium (E-CM) with cultured human umbilical vein
endothelial cells (HUVEC), resulted in a fivefold increased formation
of thiobarbituric acid-reactive substances (TBARS) and activation of
the transcription factor NF-kB, both indicators of cellular oxidant
stress. Normal RBC show none of these phenomena. The oxidant
stress-induced signaling resulted in an increased surface expression of
a subset of CAMs, ICAM-1, E-selectin, and VCAM-1 in HUVEC. The addition
of oxygen radical scavenger enzymes (catalase, superoxide dismutase)
and antioxidant (probucol) inhibited these events. Additionally,
preincubation of HUVEC with a synthetic peptide Arg-Gly-Asp (RGD) that
prevents vWf-mediated adhesion of SS RBC reduced the surface expression of VCAM-1 and NF-kB activation. Furthermore, SS RBC-induced oxidant stress resulted in a twofold increase in the transendothelial migration
of both monocyte-like HL-60 cells and human peripheral blood monocytes,
and approximately a sixfold increase in platelet-endothelial cell
adhesion molecule-1 (PECAM-1) phosphorylation, each of which was
blocked by protein kinase C inhibitor and antioxidants. These results
suggest that the adherence/contact of SS RBC to endothelial cells in
large vessel can generate enhanced oxidant stress leading to increased
adhesion and diapedesis of monocytes, as well as heightened adherence
of SS reticulocytes, indicating that injury/activation of endothelium
can contribute to vaso-occlusion in SCD.
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