Tenascin is highly expressed in endometriosis and its expression is upregulated by estrogen

ObjectiveTo investigate the localization of tenascin expression in the endometrium of women without endometriosis and in endometriotic implants, and to determine the in vitro regulation of tenascin by E2 in these tissues.DesignExperimental laboratory study.SettingUniversity medical center.Patient(s)Reproductive age women with or without endometriosis.Intervention(s)Proliferative (n = 14), and secretory (n = 14) endometrium from women without endometriosis and endometriosis implants (n = 14) were used for immunohistochemical analysis. Endometrial and endometriotic stromal cells were grown in culture and treated with E2, the estrogen receptor antagonist ICI 182 780 (ICI) alone, E2 in combination with ICI, or vehicle (control) for 24 hours, and tenascin expression was analyzed by Western blotting.Main Outcome Measure(s)Expression levels of tenascin in normal endometrium and endometriotic implants and its regulation by E2.Result(s)Tenascin immunostaining revealed an increasing intensity in the stromal cells, starting from normal secretory endometrium, then normal proliferative endometrium, and reaching the highest expression in endometriotic implants. Estradiol induced a significant increase in tenascin protein levels in the endometriotic stromal cells in culture.Conclusion(s)The modulation of tenascin as an extracellular matrix protein by E2 in endometriotic stromal cells may be one of the factors playing a role in the development of endometriosis. To investigate the localization of tenascin expression in the endometrium of women without endometriosis and in endometriotic implants, and to determine the in vitro regulation of tenascin by E2 in these tissues. Experimental laboratory study. University medical center. Reproductive age women with or without endometriosis. Proliferative (n = 14), and secretory (n = 14) endometrium from women without endometriosis and endometriosis implants (n = 14) were used for immunohistochemical analysis. Endometrial and endometriotic stromal cells were grown in culture and treated with E2, the estrogen receptor antagonist ICI 182 780 (ICI) alone, E2 in combination with ICI, or vehicle (control) for 24 hours, and tenascin expression was analyzed by Western blotting. Expression levels of tenascin in normal endometrium and endometriotic implants and its regulation by E2. Tenascin immunostaining revealed an increasing intensity in the stromal cells, starting from normal secretory endometrium, then normal proliferative endometrium, and reaching the highest expression in endometriotic implants. Estradiol induced a significant increase in tenascin protein levels in the endometriotic stromal cells in culture. The modulation of tenascin as an extracellular matrix protein by E2 in endometriotic stromal cells may be one of the factors playing a role in the development of endometriosis.