Expression and significance of ERβ and TrkB in endometriosis

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This study found that ERβ, TrkB, and BDNF were more highly expressed in ectopic endometrial tissue than eutopic tissue from endometriosis patients, while ERα and SGPL1 showed the opposite expression pattern.

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This study investigated potential mechanisms in endometriosis by measuring expression of estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), tyrosine kinase receptor type B (TrkB), and related molecules BDNF and SGPL1 in tissues from patients with endometriosis, using real-time PCR, western blot, and immunohistochemistry. The authors found ERα and SGPL1 mainly in eutopic endometrium compared with ectopic endometrium, whereas ERβ, BDNF, and TrkB were higher in ectopic endometrium, and ERβ (cytoplasmic) was the focus of their proposed pathogenesis contribution. They also reported that ERβ, ERα, TrkB, and SGPL1 protein levels were higher in the proliferative phase than in the secretory phase in eutopic endometrium, and that TrkB, BDNF, and SGPL1 were not detected in control endometrium. This paper is centrally about endometriosis—specifically the expression and significance of ERβ and TrkB in endometriotic tissues and their association with ectopic versus eutopic endometrium.

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Abstract

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.
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Abstract

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.

Keywords

- Endometriosis (EMs) - Estrogen receptor-α (ERα) - Estrogen receptor-β (ERβ) - Tyrosine kinase receptor B (TrkB) - Brainderived neurotrophic factor (BDNF) - Immunohistochemistry (IHC)

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Estrogen Receptor beta Gene Expression Regulation Receptor, trkB Uterine Diseases Blotting, Western Endometriosis Endometriosis Estrogen Receptor beta Estrogen Receptor beta Female Humans Immunohistochemistry Real-Time Polymerase Chain Reaction Receptor, trkB Receptor, trkB RNA RNA Uterine Diseases Uterine Diseases

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europepmc
last seen: 2026-06-13T06:22:48.782012+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
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