Dipyridamole inhibits O2- release and expression of tissue factor activity by peripheral blood monocytes stimulated with lipopolysaccharide

John P. Brozna, Marilee Horan, Steven D. Carson

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

Monocytes can be induced to synthesize and express tissue factor procoagulant activity. They can also be stimulated to release a broad spectrum of inflammatory agents including superoxide anion (O2-) that are thought to contribute to the pathogenesis of inflammatory diseases. Dipyridamole, an inhibitor of platelet aggregation blocks the lipopolysaccharide (LPS) - induced increase in monocyte-associated tissue factor activity and phorbol myristate acetate (PMA) stimulated O2- release from monocytes and polymorphonuclear leukocytes (PMN). Dipyridamole inhibition of O2- release can be reversed by increased glucose in the culture media, whereas dipyridamole inhibition of tissue factor can not be reversed by increased glucose in the culture media. These results reveal that dipyridamole influences monocytes by at least two distinct mechanisms. Further, it may serve as an anti-thrombotic agent by virtue of its effect on both platelet aggregation and monocyte tissue factor activity1.

Original languageEnglish (US)
Pages (from-to)141-156
Number of pages16
JournalThrombosis Research
Volume60
Issue number2
DOIs
StatePublished - Oct 15 1990

Keywords

  • dipyridamole
  • monocytes
  • tissue factor

ASJC Scopus subject areas

  • Hematology

Fingerprint Dive into the research topics of 'Dipyridamole inhibits O<sub>2</sub><sup>-</sup> release and expression of tissue factor activity by peripheral blood monocytes stimulated with lipopolysaccharide'. Together they form a unique fingerprint.

Cite this