Estrogen signaling in the proliferative endometrium: implications in endometriosis

Silva, Rita de Cássia Pereira da Costa e; Moura, Kátia Karina Verolli de Oliveira; Júnior, C.L. Ribeiro; Guillo, Lidia Andreu

doi:10.1590/1806-9282.62.01.72

Cited by 18 publications

(16 citation statements)

References 45 publications

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“…In the normal human endometrium, eNOS is regulated by estrogen and progesterone (Han et al, 2005;Khorram et al, 2009;Silva et al, 2016) and is expressed in the glandular and endometrial microvascular epithelium during the luteal phase (Cameron and Campbell et al, 1998). Therefore, synthesis of adequate NO levels is required for proper hormonal signaling.…”

Section: Discussionmentioning

confidence: 99%

Research Article Endothelial nitric oxide synthase G894T polymorphism increases the risk of infertility in women with endometriosis

Silva¹,

Faria²,

Silva³

et al. 2019

Genet. Mol. Res.

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Endometriosis is a chronic disease with adverse implications for fertility. We investigated the G894T polymorphism in the endothelial nitric oxide synthase gene in fertile and infertile women with endometriosis. This prospective study included a group of 52 women with a laparoscopic diagnosis of endometriosis. DNA was extracted from blood obtained from 47 patients and analyzed by PCR. The overall cohort was divided into infertile (n = 24) and fertile (n = 23) subgroups and compared in terms of genotypic and allelic frequencies. The genotypic distribution followed Hardy-Weinberg equilibrium ( 2 = 2.21, P = 0.137) and included the GG genotype in 28/47 GT in 14/47, and TT in 5/47 of the samples. Genotypic and allelic frequencies between fertile and infertile women with endometriosis showed that absence of the TT genotype was associated with fertility in endometriosis patients (P = 0.0623). The T ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 18 (2): gmr18201 R.C.P.C. e Silva et al. 2 allele was present in 17 patients of the infertile group and 7 patients of the fertile group (P = 0.025). This allele was significantly associated with infertility (relative risk = 2.21, 95% confidence interval 1.56-3.08) for the recessive model of inheritance. Our findings suggest that women with endometriosis and the G894T polymorphism in the endothelial nitric oxide synthase gene are at increased risk of infertility.

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Section: Discussionmentioning

confidence: 99%

Research Article Endothelial nitric oxide synthase G894T polymorphism increases the risk of infertility in women with endometriosis

Silva¹,

Faria²,

Silva³

et al. 2019

Genet. Mol. Res.

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“…As it pertains to the uterus, estrogen binds to estrogen receptors (ER; alpha and beta) in the cytoplasm or nucleus of endometrial glandular and epithelial stromal cells. The resulting E2-ER complex can then directly interact with the promoter regions of specific sequences of DNA related to the G1 phase of the cell cycle and induce mitotic proliferation by regulating cyclins, cyclin-dependent kinases (cdk), and cyclin-dependent kinase inhibitors [3]. One of these cyclins includes cyclin E, which increases in concentration during the endometrial proliferative phase and in response to estrogen signaling.…”

Section: The Proliferative Phasementioning

confidence: 99%

“…Along with cdk2, cyclin E is believed to be the rate-limiting activator of G1 to S phase [4]. Other cyclins that are directly regulated by binding of the E2-ER complex include cyclin B1 and cyclin D1 [3]. Throughout the ovarian follicular phase, as serum estrogen levels continue to rise in response to folliculogenesis, the transcription of cell cycle-related genes in the endometrial tissue increases.…”

Section: The Proliferative Phasementioning

confidence: 99%

Implantation: Cross Talk of the Developing Embryo and Endometrium

Grimm¹,

Cooper²,

Beltsos³

et al. 2020

Innovations in Assisted Reproduction Technology

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The window of implantation has long posed as a challenge in understanding the exact synchronized cross talk that must take place in order for a developing embryo to be appropriately received by the endometrium. This is due mostly to the fact that it is difficult to study human models of implantation without sacrificing the potential for pregnancy. For many who present with a diagnosis of infertility with an otherwise unexplained etiology, recurrent implantation failure or a displaced window of receptivity may be an underlying, silent cause. As assisted reproductive technology (ART) continues to advance and offer new scientific breakthroughs allowing greater insight and understanding to reproductive failure and infertility, endometrial receptivity testing may offer answers to struggling patients.

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“…5,6 Oestrogen fuels the cell proliferation, promotes inflammation and inhibits apoptosis, and it is regarded as one of the factors that promotes the development of endometriosis. [7][8][9] Studies found that aromatase and oestrogen kept high level in endometriosis tissues and survived the cells in ectopic locations. 10,11 Furthermore, other studies have reported the aberrant level of EMT is present in endometriosis and oestrogen induces cell proliferation, invasion, migration and EMT-related markers in both normal and endometriotic epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

RhoA/ROCK pathway mediates the effect of oestrogen on regulating epithelial‐mesenchymal transition and proliferation in endometriosis

Huang

Mao

et al. 2020

J Cellular Molecular Medi

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Endometriosis is a benign gynaecological disease appearing with pelvic pain, rising dysmenorrhoea and infertility seriously impacting on 10% of reproductive‐age females. This research attempts to demonstrate the function and molecular mechanism of RhoA/ROCK pathway on epithelial‐mesenchymal transition (EMT) and proliferation in endometriosis. The expression of Rho family was abnormally changed in endometriotic lesions; in particular, RhoA and ROCK1/2 were significantly elevated. Overexpression of RhoA in human eutopic endometrial epithelial cells (eutopic EECs) enhanced the cell mobility, epithelial‐mesenchymal transition (EMT) and proliferation, and RhoA knockdown exhibited the opposite function. Oestrogen up‐regulated the RhoA activity and expression of RhoA and ROCK1/2. RhoA overexpression reinforced the effect of oestrogen on promoting EMT and proliferation, and RhoA knockdown impaired the effect of oestrogen. oestrogen receptor α (ERα) was involved with the regulation of oestrogen on EMT and proliferation and up‐regulated RhoA activity and expression of RhoA and ROCK1/2. The function of ERα was modulated by the change in RhoA expression. Furthermore, phosphorylated ERK that was enhanced by oestrogen and ERα promoted the protein expression of RhoA/ROCK pathway. Endometriosis mouse model revealed that oestrogen enhanced the size and weight of endometriotic lesions. The expression of RhoA and phosphorylated ERK in mouse endometriotic lesions was significantly elevated by oestrogen. We conclude that abnormal activated RhoA/ROCK pathway in endometriosis is responsible for the function of oestrogen/ERα/ERK signalling, which promoted EMT and proliferation and resulted in the development of endometriosis.

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Estrogen signaling in the proliferative endometrium: implications in endometriosis

Cited by 18 publications

References 45 publications

Research Article Endothelial nitric oxide synthase G894T polymorphism increases the risk of infertility in women with endometriosis

Research Article Endothelial nitric oxide synthase G894T polymorphism increases the risk of infertility in women with endometriosis

Implantation: Cross Talk of the Developing Embryo and Endometrium

RhoA/ROCK pathway mediates the effect of oestrogen on regulating epithelial‐mesenchymal transition and proliferation in endometriosis

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