P-Selectin-mediated acute inflammation can be blocked by chemically modified heparin, RO-heparin

Mol Cells. 2005 Jun 30;19(3):350-5.

Abstract

Selectins are carbohydrate-binding cell adhesion molecules that play a major role in the initiation of inflammatory responses. Heparin can bind to P-selectin, and its anti-inflammatory property is mainly due to inhibition of P-selectin. However, the strong anticoagulant activity of heparin limits its clinical use. We prepared periodate-oxidized, borohydride-reduced heparin (RO-heparin) by chemical modification and tested its anticoagulant and anti-inflammatory activities. Activated partial thromboplastin time (aPTT) assays showed that, compared with heparin, RO-heparin had greatly reduced anticoagulant activity. Intravenous administration of this compound led to reduction in the peritoneal infiltration of neutrophils in a mouse acute inflammation model. In vitro cell adhesion experiments demonstrated that the effect of RO-heparin on inflammatory responses was mainly due to inhibiting the interaction of P-selectin with its ligands. These results indicate that RO-heparin may be a safer treatment for inflammation than heparin, especially when selectin is targeted.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anticoagulants / pharmacology
  • Endothelium, Vascular / cytology
  • HL-60 Cells
  • Heparin / analogs & derivatives*
  • Heparin / chemistry*
  • Heparin / pharmacology*
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Oxidation-Reduction
  • P-Selectin*
  • Peritonitis / chemically induced
  • Peritonitis / prevention & control*

Substances

  • Anticoagulants
  • P-Selectin
  • RO-heparin
  • Heparin