Sickle hemoglobin (HbS) polymerizes under decreased oxygen conditions leading to alterations in erythrocyte physiology in patients with sickle cell disease (SCD). One of the many complications resulting from SCD is vascular inflammation caused by the release of free heme from sickle erythrocytes and a constant cycle of ischemia/reperfusion. Released heme activates toll-like receptor 4 (TLR4) leading to the activation of the pro-inflammatory NF-kB transcription factor and the expression of adhesion molecules, such as P-selectin and von Willebrand factor (vWF), which promote vaso-occlusion. Previous research indicates that the formation of the TLR4 complex requires the removal of α-2,3 sialyl residues from TLR4 by Neuraminidase-1. We hypothesize that treatment of human umbilical vein endothelial cells with a bacterial neuraminidase, prior to treatment with heme or LPS, will enhance TLR4 activation of NF-kB and cell-surface expression of P-selectin and von Willebrand factor. We measured vWF and P-selectin on endothelial cells stimulated with heme or LPS with and without neuraminidase. We found that treatment of endothelial cells with a neuraminidase does not lead to significant increases in vWF and P-selectin expression.

Endothelial cell-associated sialic acid and sickle cell disease

2019 Spring National Meeting

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