Platelet-erythrocyte adhesion in sickle cell disease

Theodore Wun, Teresa Paglieroni, Cara L. Field, Jeanna L Welborn, Anthony Cheunt, Naomi J. Walker, Fern Tablin

Research output: Contribution to journalArticlepeer-review

51 Scopus citations


Background: The abnormal adherence of sickle red blood cells (sRBC) to other cell types likely contributes to vasoocclusion. Increased numbers of platelet-erythrocyte aggregates (PEA) and platelet activation have been described in sickle cell disease. The present study was undertaken to determine the contribution, if any, of the extracellular matrix protein thrombospondin to the adhesion of sRBC and platelets. Methods: Platelet activation and PEA were measured using fluoresecent-labeled monoclonal antibodies and flow cytometry. Platelet red-cell adhesion was measured by a gravity sedimentation assay. Erythrocyte-bound thrombospondin (TSP) was determined by enzyme-linked immunoabsorbant assay (ELISA). Results: Our studies demonstrate significant platelet activation and adhesion of sRBC to platelets in sickle cell disease. Thrombospondin was detected on sRBC. There was variable inhibition of sRBC-platelet adhesion by antibodies to CD36 (thrombospondin receptor) and antibodies to thrombospondin. Conclusions: Thrombospondin on sRBC may mediate, at least in part, sRBC-platelet adhesion in sickle cell disease. The study of heterotypic cell-cell interactions is important in understanding the pathogenesis of vaso-occlusion in sickle cell disease.

Original languageEnglish (US)
Pages (from-to)121-127
Number of pages7
JournalJournal of Investigative Medicine
Issue number3
StatePublished - Mar 1999


  • CD 36
  • Platelet-erythrocyte aggregates
  • Platelets
  • Sickle cell disease
  • Thrombospondin

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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