Estrogen, inflammation, and platelet phenotype

Virginia M. Miller, Muthuvel Jayachandran, Kazumori Hashimoto, John A. Heit, Whyte G. Owen

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


Background: Although exogenous estrogenic therapies increase the risk of thrombosis, the effects of estrogen on formed elements of blood are uncertain. Objective: This article examines the genomic and nongenomic actions of estrogen on platelet phenotype that may contribute to increased thrombotic risk. Methods: To determine aggregation, secretion, protein expression, and thrombin generation, platelets were collected from experimental animals of varying hormonal status and from women enrolled in the Kronos Early Estrogen Prevention Study. Results: Estrogen receptor β predominates in circulating platelets. Estrogenic treatment in ovariectomized animals decreased platelet aggregation and adenosine triphosphate (ATP) secretion. However, acute exposure to 17β-estradiol did not reverse decreases in platelet ATP secretion invoked by lipopolysaccharide. Thrombin generation was positively correlated to the number of circulating microvesicles expressing phosphatidylserine. Conclusion: Assessing the effect of estrogen treatments on blood platelets may lead to new ways of identifying women at risk for adverse thrombotic events with such therapies.

Original languageEnglish (US)
Pages (from-to)S91-S102
JournalGender Medicine
Issue numberSUPPL. 1
StatePublished - 2008


  • 17β-estradiol
  • LPS
  • TLR4
  • estrogen
  • lipopolysaccharide
  • microvesicles
  • testosterone

ASJC Scopus subject areas

  • Gender Studies


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