Modulation of Sickle Red Blood Cell Adhesion and its Associated Changes in Biomarkers by Sulfated Nonanticoagulant Heparin Derivative. (April 2016)

• Record Type: Journal Article
• Authors: Alshaiban, Abdulelah; Muralidharan-Chari, Vandhana; Nepo, Anne; Mousa, Shaker A.
• Is Part Of: Clinical and applied thrombosis/hemostasis. Volume 22:Number 3(2016)
• Page Start: 230
• Page End: 238
• Publication Date: 2016-04
• Subjects: sickle cell disease -- sickle red blood cells -- endothelial cells -- adhesion molecules -- selectin -- ICAM-1 -- heparin -- tinzaparin -- sulfated nonanticoagulant heparin; Hemostasis -- Periodicals; Thrombosis -- Periodicals; 616.13
• DOI: 10.1177/1076029614565880
• Languages: English
• ISSNs: 1076-0296

Abstract

Abnormal cellular adhesion is one of the primary causes of vaso-occlusive crisis in sickle cell disease (SCD). Levels of intercellular adhesion molecule 1 (ICAM-1) and P-selectin are upregulated, resulting in increased adhesion of leukocytes and sickle red blood cells (RBCs) to endothelium. This study compares the inhibitory effect of a sulfated nonanticoagulant heparin (S-NACH) derivative with a low-molecular-weight heparin, tinzaparin, on the adhesion of sickle RBCs to endothelium. The S-NACH exhibits minimum effects on hemostasis and bleeding and interferes with the binding of pancreatic cancer cells to endothelial cells via P-selectin. We show by static binding assay that pretreatment of both erythrocytes and endothelial cells with S-NACH significantly inhibits the increased adhesion of sickle RBCs to endothelial cells. The S-NACH treatment also decreases the higher plasma levels of (adhesion biomarkers) ICAM-1 and P-selectin in SCD mice. This investigation signals further research into the potential use of S-NACH in treating vaso-occlusions with minimal bleeding events in patients with SCD.