OBJECTIVES: To study the potential pathogenesis of endometriosis (EMs) in an area of estrogen receptors (ERs) and tyrosine kinase receptor type B (TrkB) expressions in tissues from patients with EMs. STUDY DESIGN: The authors examined the expressions of ERα, ERβ, TrkB, brain-derived neurotrophic factor (BDNF), and SGPL1 in tissues with EMs, using real-time PCR, western blot, and immunohistochemistry. RESULTS: ERα and SGPL1 were mainly expressed in eutopic endometrium than that in ectopic endometrium of patients with ovarian endometriosis (p < 0.05), while ERβ, BDNF, and TrkB were adverse, mainly detected in ectopic endometrium of the same patients with EMs (p < 0.01 and p < 0.05 ) by real-time PCR and western blot. ERβ, ERα, TrkB, and SGPL1 proteins were mainly expressed in eutopic endometrium of proliferative phase with EMs than that in eutopic endometrium of secretory phase (p < 0.05 ). TrkB, BDNF, and SGPL1 were not found in endometrium of proliferative or secretory phase in control group. CONCLUSIONS: ERβ expressed in cytoplasm may mediate pathogenesis of EMs.
OBJECTIVES: To study the potential pathogenesis of endometriosis (EMs) in an area of estrogen receptors (ERs) and tyrosine kinase receptor type B (TrkB) expressions in tissues from patients with EMs. STUDY DESIGN: The authors examined the expressions of ERα, ERβ, TrkB, brain-derived neurotrophic factor (BDNF), and SGPL1 in tissues with EMs, using real-time PCR, western blot, and immunohistochemistry. RESULTS: ERα and SGPL1 were mainly expressed in eutopic endometrium than that in ectopic endometrium of patients with ovarian endometriosis (p < 0.05), while ERβ, BDNF, and TrkB were adverse, mainly detected in ectopic endometrium of the same patients with EMs (p < 0.01 and p < 0.05 ) by real-time PCR and western blot. ERβ, ERα, TrkB, and SGPL1 proteins were mainly expressed in eutopic endometrium of proliferative phase with EMs than that in eutopic endometrium of secretory phase (p < 0.05 ). TrkB, BDNF, and SGPL1 were not found in endometrium of proliferative or secretory phase in control group. CONCLUSIONS: ERβ expressed in cytoplasm may mediate pathogenesis of EMs.