Estrogen Receptor-β, Estrogen Receptor-α, and Progesterone Resistance in Endometriosis

Bulun, Serdar E.; Cheng, You; Pavone, Mary Ellen; Xue, Qing; Attar, Erkut; Trukhacheva, Elena; Tokunaga, Hideki; Utsunomiya, Hiroki; Yin, Ping; Luo, Xia; Lin, Zhihong; İmir, Gonca; Thung, Stephen; Su, Emily J.; Kim, Julie

doi:10.1055/s-0029-1242991

Cited by 221 publications

(180 citation statements)

References 54 publications

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“…The estrogen plays an important role in the planting and growth of ectopic endometrium (Burney & Giudice 2012). Loss of P 4 signaling in the endometrium may be a causal factor in the development of EMS, and P 4 resistance is commonly observed in women with this disease (Bulun et al 2010). Tsutsumi et al (2011) reported that medroxyprogesterone acetate almost completely antagonized the E 2 -induced CXCL12 production in normal ESCs.…”

Section: Discussionmentioning

confidence: 99%

The role of SRC1 and SRC2 in steroid-induced SDF1 expression in normal and ectopic endometrium

Shi

Dai

et al. 2014

Reproduction

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To compare the expression patterns of steroid receptor coactivators (SRCs) and steroid-induced stromal cell-derived factor 1 (CXCL12 (SDF1)) in normal and ectopic endometrium and to explore the roles of NCOA1 (SRC1) and NCOA2 (SRC2) in the steroid-induced CXCL12 expression in normal and ectopic endometrial stromal cells (ESCs). The NCOA1, NCOA2, NCOA3 (SRC3), and CXCL12 (SDF1)a mRNA levels in normal and ectopic endometrium were analyzed by quantitative real-time PCR. Steroid-induced CXCL12 expression was detected by the ELISA method and the chemotactic activity of conditioned supernatant to monocyte was assessed by the Boyden chamber method before and after the silencing of NCOA1 or NCOA2 with siRNA in normal and ectopic ESCs. The expression of NCOA1 and CXCL12 in ectopic endometrium was significantly greater than that in normal endometrium in the secretory phase. Progesterone (P 4 ) was able to significantly inhibit estradiol (E 2 )-stimulated CXCL12 expression in normal and ectopic ESCs. The inhibitory rate of P 4 in ectopic ESCs at 72 and 96 h was significantly lower than that in normal ESCs. Silencing of NCOA1 but not NCOA2 significantly reduced the E 2 -induced CXCL12 expression in normal and ectopic ESCs. The ability of P 4 to inhibit E 2 -induced CXCL12 expression and monocyte chemotaxis in normal and ectopic ESCs was significantly attenuated when NCOA2 was silenced. NCOA1 plays a necessary role in E 2 -induced CXCL12 expression and NCOA2 is required for P 4 to inhibit the E 2 -induced CXCL12 production in normal and ectopic endometrium.

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Section: Discussionmentioning

confidence: 99%

The role of SRC1 and SRC2 in steroid-induced SDF1 expression in normal and ectopic endometrium

Shi

Dai

et al. 2014

Reproduction

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“…Endometriyumda progesteron sinyalinin kaybolması, endometriyozis gelişmesine neden olan bir faktör olabilir ve progesteron direnci geliştiğinden, uzun süreli progestin tedavisine yanıt oluşturmaz. 16 Selektif östro-jen reseptör modülatörler (SERM), farklı dokularda ER'ye bağlanarak agonist veya antagonist etki gös-terirler. Endometriyum üzerinde antagonist etki yaparlar.…”

Section: Selekti̇f öStrojen Reseptör Modülatörleri̇unclassified

Treatment of Endometriosis with Non-Hormonal Agents: Review

Özdemirci¹,

Dilbaz²

2016

Turkiye Klinikleri J Gynecol Obst

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“…The initial event may involve deficient methylation of the estrogen receptor ERβ promoter resulting in pathologic overexpression of ERβ in endometriotic stromal cells. Ιt is postulated that alterations in the relative levels of ERβ and ERα in endometrial tissue dictate estradiol-regulated progesterone receptor (PR) expression, such that a decreased ERα-to-ERβ ratio may result in suppression of PR [80]. Based on observations regarding the the etiopathogenesis of the disease, scientific work has been done to confirm suspicions that human endometriosis may result from toxic exposure [81,82].…”

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confidence: 99%

Adverse Effects on Female Human Reproductive Health from Exposure to Endocrine Disruptors: Focus on Endometrial Lesions

Karoutsou¹,

Karoutsos²,

Karoutsos³

2016

J Clin Epigenet

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It is currently apparent that the intentional release of compounds through agricultural, industrial, and municipal activities has influenced the health of wildlife and human populations. Scientists are invited to study disturbances in the normal function of the reproductive system of genetically modified populations. When referring to a population, they rather use the term control or reference; the reason is an enormous rate of information concerning the endocrine-altering potential of plasticizers and dyes, as well as the possible influences of pesticides and industrial compounds on various endocrine endpoints, particularly regarding the concentration of estrogens. Here in, we provide an overview on the impact of chemical substances on female human reproductive health.

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Estrogen Receptor-β, Estrogen Receptor-α, and Progesterone Resistance in Endometriosis

Cited by 221 publications

References 54 publications

The role of SRC1 and SRC2 in steroid-induced SDF1 expression in normal and ectopic endometrium

The role of SRC1 and SRC2 in steroid-induced SDF1 expression in normal and ectopic endometrium

Treatment of Endometriosis with Non-Hormonal Agents: Review

Adverse Effects on Female Human Reproductive Health from Exposure to Endocrine Disruptors: Focus on Endometrial Lesions

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