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Blood, 1 April 2001, Vol. 97, No. 7, pp. 1937-1941
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Modulation of endothelial cell activation in sickle cell disease:
a pilot study
Alex A. Solovey,
Anna N. Solovey,
Jeanne Harkness, and
Robert P. Hebbel
From the Department of Medicine, University of
Minnesota Medical School, Minneapolis.
The vessel wall endothelium undoubtedly plays a role in the
vascular pathobiology of sickle cell disease. This pilot study tested
the feasibility of using an inhibitor of nuclear factor (NF)- B, a
transcription factor, to modify the endothelial activation state
of patients with this vascular disease. For a total of 7 separate
drug exposure tests, 3 subjects with sickle cell disease took
sulfasalazine (given orally at 1 g every 8 hours), and the activation state of their circulating endothelial cells (CECs) was
assessed using immunofluorescence microscopy. Companion studies were
also performed using sulfasalazine in sickle transgenic mice to
verify its effect simultaneously on both CECs and vessel wall endothelium. Both CECs and tissue vessel wall endothelium in sickle mice have an activated phenotype. In these mice sulfasalazine significantly reduced CEC expression of vascular cell adhesion molecule
(VCAM), intracellular adhesion molecule (ICAM), and E-selectin, and it
correspondingly reduced expression of these molecules in some tissue
vessels. In humans with sickle cell disease, sulfasalazine significantly reduced CEC expression of VCAM, ICAM, and E-selectin, but
it did not reduce expression of tissue factor. Addition of a second
transcription factor inhibitor, salsalate, did not change this result.
This pilot study suggests that endothelial cell activation state
can be modified and down-regulated in vivo by sulfasalazine.
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