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Blood, Vol. 93 No. 4 (February 15), 1999:
pp. 1422-1429
Anionic Polysaccharides Inhibit Adhesion of Sickle Erythrocytes to
the Vascular Endothelium and Result in Improved Hemodynamic Behavior
G.A. Barabino,
X.D. Liu,
B.M. Ewenstein, and
D.K. Kaul
From the Department of Chemical Engineering, Northeastern University,
Boston, MA; the Department of Medicine, Albert Einstein College of
Medicine, Bronx, NY; and the Hematology Division, Brigham & Women's
Hospital, Boston, MA.
The abnormal adherence of sickle red blood cells (SS RBC) to
vascular endothelium may play an important role in vasoocclusion in
sickle cell anemia. Thrombospondin (TSP), unusually large molecular weight forms of von Willebrand factor, and laminin are known to enhance
adhesion of SS RBC. Also, these endothelial proteins bind to sulfated
glycolipids and this binding is inhibited by anionic polysaccharides.
Reversible sickling may expose normally cryptic membrane sulfatides
that could mediate this adhesive interaction. In this study, we have
investigated the effect of anionic polysaccharides, in the presence or
absence of TSP, on SS RBC adhesion to the endothelium, using cultured
human umbilical vein endothelial cells (HUVEC) (for the adhesion assay)
and the ex vivo mesocecum of the rat (for hemodynamic evaluation). The
baseline adhesion (ie, without added TSP) of SS RBC to HUVEC was most
effectively inhibited by high molecular weight dextran sulfate (HDS),
whereas low molecular weight dextran sulfate (LDS) and the
glycosaminoglycan chondroitin sulfate A (CSA) also had significant
inhibitory effects. Heparin was mildly effective whereas other
glycosaminoglycans (chondroitin sulfates B and C, heparan sulfate, and
fucoidan) were ineffective. Similarly, HDS and CSA resulted in an
improved hemodynamic behavior of SS RBC. Soluble TSP caused significant
increases in SS RBC adhesion and in the peripheral resistance. Both HDS
and CSA prevented TSP-enhanced adhesion and hemodynamic abnormalities.
Thus, anionic polysaccharides can inhibit SS RBC-endothelium
interaction in the presence or absence of soluble TSP. These agents may
interact with RBC membrane component(s) and prevent TSP-mediated
adhesion of SS RBC to the endothelium.
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