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Blood, 1 January 2005, Vol. 105, No. 1, pp. 115-121. Prepublished online as a Blood First Edition Paper on June 15, 2004; DOI 10.1182/blood-2003-11-3840. This Article Full Text (PDF) All Versions of this Article: 2003-11-3840v1 105/1/115    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Moro, L. Articles by Sinigaglia, F. Search for Related Content PubMed PubMed Citation Articles by Moro, L. Articles by Sinigaglia, F. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 12, 2003 Accepted May 20, 2004 Non-genomic effects of 17-estradiol in human platelets: potentiation of thrombin-induced aggregation through estrogen receptor and Src kinase Laura Moro, Stefania Reineri, Daniela Piranda, Daniela Pietrapiana, Paolo Lova, Alessandra Bertoni, Andrea Graziani, Paola Defilippi, Ilaria Canobbio, Mauro Torti, and Fabiola Sinigaglia* DISCAFF, University 'A. Avogadro', Novara, Italy Department of Medical Sciences, University 'A. Avogadro', Novara, Italy; DISCAFF, University 'A. Avogadro', Novara, Italy Department of Medical Sciences, University 'A. Avogadro', Novara, Italy Department of Biochemistry, University of Pavia, Pavia, Italy Department of Genetics, Biology and Biochemistry, University of Turin, Turin, Italy * Corresponding author; email: fabiola.sinigaglia{at}med.unipmn.it. The impact of estrogens on the cardiovascular system, and their ability to regulate platelet function is controversial. The recent finding that estrogen receptors are expressed in human platelets renders these cells an excellent model to study the non-genomic effects of these hormones. In this work, we investigated the 17-estradiol-dependent signaling in platelets from adult healthy men. 17-estradiol caused the rapid phosphorylation of the tyrosine kinases Src and Pyk2, and the formation of a signaling complex, which included Src, Pyk2, and the phosphatidylinositol 3-kinase. Both these events were dependent on estrogen receptor engagement. We found that estrogen receptor was membrane associated in platelets, and, upon treatment with 17-estradiol, activation of Src and Pyk2 occurred in the membrane fraction, but not in the cytosol. By contrast, no significant activation of phosphatidylinositol 3-kinase was detected in estrogen-treated platelets. 17-estradiol did not induce any platelet response directly, but strongly potentiated both activation of integrin IIb3 and platelet aggregation induced by subthreshold concentrations of thrombin. These effects were dependent on estrogen receptor recruitment, and were associated with a strong synergistic effect with thrombin on Src activation. Taken together, these results indicate that 17-estradiol can modulate platelet functions by exercising a pro-aggregating role. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. E. Toutain, C. Filipe, A. Billon, C. Fontaine, L. Brouchet, J.-C. Guery, P. Gourdy, J.-F. Arnal, and F. 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