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Blood, 1 March 2002, Vol. 99, No. 5, pp. 1564-1571
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Role of erythrocyte phosphatidylserine in sickle red
cell-endothelial adhesion
B. N. Yamaja Setty,
Surekha Kulkarni, and
Marie J. Stuart
From the Division of Research Hematology, Department of
Pediatrics, Jefferson Medical College, Thomas Jefferson University and
the Marian Anderson Comprehensive Sickle Cell Center, Philadelphia, PA.
Phosphatidlyserine (PS) exposure on the erythrocyte surface endows
the cell with the propensity of adhering to vascular endothelium. Because individuals with sickle cell disease (SCD) manifest loss of
erythrocyte membrane asymmetry with PS exposure, we have assessed the
contribution of this marker to the process of sickle
erythrocyte-microendothelial adhesion. Assays for plasma-induced
adhesion were conducted on unactivated endothelium, in the absence of
immobilized ligands, such that PS was compared to the erythrocyte
adhesion receptor CD36. Blocking studies with erythrocytes pretreated
with annexin V (to cloak PS) or anti-CD36 or both revealed an
inhibitory effect on adhesion of 36% ± 10% and 23% ± 8% with
blocking of both sites suggestive of an additive effect. We next
evaluated 87 blood samples from patients with SCD and grouped them into
4 categories based on adhesion marker (CD36 and PS) levels. Results
revealed a striking correlation between erythrocyte PS positivity and
adhesion. Analyses of the individual patient data demonstrated a
positive correlation between PS and adhesion (R = 0.52,
P < .000 001), whereas none was noted between adhesion
and CD36 (R = 0.2, P > .07). The effect of PS on
adhesion appears to be related to the quantitative differences in
erythrocyte markers in SCD, with PS the predominant marker when
compared to CD36 both in the total erythrocyte population, and when the
adherence-prone erythrocyte, the CD71+ stress reticulocyte,
was evaluated. Our study signals the entrance of an important new
contributor to the field of sickle erythrocyte-endothelial adhesion.
The implications of erythrocyte PS exposure in relation to the vascular
pathology of SCD need to be assessed.
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