The pooled sensitivity and specificity in endometriosis were .79 (.71, .86) and .89 (.82, .94) for aromatase, .30 (.18, .46) and .80 (.65, .90) for human chorionic gonadotropin/luteinizing hormone receptor, .75 (.66, .83) and .47 (.34, .60) for estrogen receptor (ER)-α, .65 (.56, .74) and .68 (.55, .80) for ER-β, .45 (.38-.52) and .92 (.85-.97) for serum prolactin, .69 (.51, .83) and .30 (.16, .49) for estrogen sulfotransferase, and .73 (.60-.84) and .48 (.33-.63) for 17β-hydroxysteroid dehydrogenase type 2 (17βHSD2).
Therefore, nuclear ERβ-regulated gene networks provide critical clues to understand the molecular etiology and complexity of endometriosis and endometriosis-associated endometrial dysfunction.
Mitochondrial translocation of estrogen receptor β affords resistance to oxidative insult-induced apoptosis and contributes to the pathogenesis of endometriosis.
We therefore aimed to characterize the expression of ovarian steroid hormone receptors for estrogen alpha (ESR1), estrogen beta (ESR2), and progesterone (PGR) in different types of endometriotic lesions and eutopic endometrium from women with endometriosis and controls using a tissue microarray (TMA).
These data indicated that DMPA could upregulate the expressions of PRA/B and down-regulate ERα and ERβ in endometria but not in cyst walls from women with endometriosis.
Recent studies highlighted in this focused review linked ERβ to dysregulation of apoptotic and inflammatory networks involving novel interacting partners in endometriosis.
These epigenetic changes along with differential binding of ERβ (as a transcription factor) in CYP19A1 promoters may impair follicular steroidogenesis, leading to poor Oocyte and embryo condition in endometriosis patients.
Defective CpG methylation affecting several genes that encode key transcription factors such as GATA6, steroidogenic factor-1, and estrogen receptor-β in endometriosis gives rise to overproduction of local estrogen and prostaglandins and suppression of progesterone receptor.
Our results revealed that the positive ratio of ER-β expression was gradually reduced during the malignant transformation from endometriosis to atypical endometriosis to clear cell carcinoma.
In the present study, we performed a meta-analysis to clarify the associations between the ER-βrs4986938 and rs1256049 polymorphisms and endometriosis risk.
No association was found with ESR1 (rs1159327 A/G, rs3020348 A/C) and ESR2 (rs17179740 A/G) either for endometriosis or endometriosis-related infertility.
Because estrogen receptor (ER)β levels in endometriosis are >100 times higher than those in endometrial tissue, this review focuses on this nuclear receptor.
Genetic variants in ESR1, ESR2, and HSD17B1 genes could modify susceptibility to endometriosis and might influence the fertility status in endometriosis patients.
We evaluated the relationship between common genetic variation and endometriosis risk, using gene-based tests and single-variant analysis of genetic polymorphisms in ESR1, ESR2, PGR, CYP17A1, CYP19A1, HSD17B1, HSD17B2, CYP1A1, CYP1A2, COMT, and GSTM1.
Granulosa cells obtained from patients with endometriosis were examined for estrogen (ER-β, ER-α) and progesterone (PR-A, PR-B) receptor mRNA expression ratio against GAPDH.
In this study, we have examined the expression of the four main ERβ transcript isoforms in human endometrial tissue in women with or without endometriosis.