Activated Platelets Induce Estrogen Receptor β Expression in Endometriotic Stromal Cells

Background/Aims: Endometriosis is viewed first and foremost as an estrogen-dependent disease, featuring not only excessive estrogen production but also aberrant expression of estrogen receptors (ERs), particularly ER beta, that mediate the estrogen action. ER beta is the predominant ER in mediating estrogen action in endometriosis, and estrogen plays a vital role in the development of endometriosis; thus, ER beta is viewed as a strong candidate for therapeutic targeting. Given our recent finding that platelets aggregate in endonnetriotic lesions, we sought to investigate whether activated platelets can upregulate ER beta. Methods: Using primary endometriotic stromal cells derived from patients with ovarian endometriomas and platelets harvested from healthy donors, we performed real-time RT-PCR analysis of mRNA abundance (n = 8) and Western blot analysis of protein expression (n = 8) of ER alpha and ER beta when co-cultured with phosphate-buffered saline, platelets, thrombin alone, and platelets plus thrombin for 48 h. Results: Treatment of endometriotic stronnal cells with activated platelets resulted in the upregulation of ER beta gene and protein expression. Conclusion: In the presence of aggregated and thus activated platelets in endometriotic lesions, ER beta, but not ER alpha, is up-regulated in endometriotic stromal cells. Our result suggests that the use of antiplatelet therapy may have potential in the treatment of endometriosis. (C) 2015 S. Karger AG, Basel