Estrogen, inflammation, and platelet phenotype

Gend Med. 2008:5 Suppl A:S91-S102. doi: 10.1016/j.genm.2008.03.009.


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 beta predominates in circulating platelets. Estrogenic treatment in ovariectomized animals decreased platelet aggregation and adenosine triphosphate (ATP) secretion. However, acute exposure to 17beta-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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Blood Platelets / metabolism*
  • Estradiol / pharmacology
  • Estrogen Receptor beta / metabolism
  • Estrogens / pharmacology
  • Genetic Predisposition to Disease
  • Humans
  • Lipopolysaccharides / pharmacology
  • Menopause / physiology
  • Platelet Aggregation / physiology
  • Receptors, Estrogen / metabolism*
  • Thrombosis / genetics
  • Thrombosis / physiopathology*
  • Toll-Like Receptor 4 / administration & dosage


  • Estrogen Receptor beta
  • Estrogens
  • Lipopolysaccharides
  • Receptors, Estrogen
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Estradiol