Expression patterns of the steroid receptor coactivator family in human ovarian endometriosis

Kumagami, Atsuko; Ito, Akiko; Yoshida-Komiya, Hiromi; Fujimori, Keiya; Sato, Akira

doi:10.1111/j.1447-0756.2010.01509.x

Cited by 15 publications

(14 citation statements)

References 27 publications

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“…We observed that there was no cyclic difference in the expression of the three SRCs in ectopic endometrium throughout the whole menstrual period. Our results are similar to the previous immunohistochemical data ( Kumagami et al 2011). The ability of P 4 to inhibit E 2 -induced CXCL12 expression and monocyte chemotaxis was greatly attenuated compared with E 2 stimulation alone when NCOA2 was silenced whether in normal ESCs or in ectopic ESCs, though the CXCL12 expression showed no significant difference between NCOA1 silencing and NCOA2 silencing in ectopic ESCs treated with E 2 CP 4 .…”

Section: Discussionsupporting

confidence: 82%

“…Several researchers have reported the expression of SRCs in normal endometrium, ectopic endometrium, and ovarian endometriotic tissue detected by immunohistochemistry and semi-quantitative RT-PCR (Suzuki et al 2010, Kumagami et al 2011. In this study, the expression patterns and levels of NCOA1, NCOA2, NCOA3, and CXCL12 in normal and ectopic endometrium during the menstrual cycle were characterized using qPCR.…”

Section: Discussionmentioning

confidence: 99%

“…The NCOA1 expression in ectopic endometrium was significantly higher than that in normal endometrium in the secretory phase. In nearly all ectopic endometrial glandular and some stromal tissues of ovary, NCOA1 was colocated with ERa (ESR1; Kumagami et al 2011). Our study adopted the siRNA-based silencing technique to evaluate the roles of NCOA1 and NCOA2 in the steroid hormone-induced expression of CXCL12.…”

Section: Discussionmentioning

confidence: 99%

“…The SRC family is composed of three distinct but functionally and structurally related members: SRC1/NCOA1, SRC2/TIF2/GRIP1, and SRC3/ RAC3/ACTR/pCIP/AIB1/TRAM1 (Oñ ate et al 1995, Xu et al 2009). The SRC family members enhanced the transcriptional activity of a variety of nuclear receptors, including ER and progesterone receptor, and are expressed in a variety of hormone-responsive tissues including the ectopic endometrium (York & O'Malley 2010, Kumagami et al 2011. In this study, we observed the expression patterns of SRCs and CXCL12 in normal and ectopic endometrium by quantitative real-time PCR (RT-qPCR) and explored the roles of NCOA1 (SRC1) and NCOA2 (SRC2) in the steroid-induced CXCL12 expression in normal and ectopic ESCs employing siRNA-based gene silencing.…”

Section: Introductionmentioning

confidence: 99%

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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: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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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“…Endometriosis is an estrogen-dependent condition marked first by ectopic endometrium typically associated with the presence of peritoneal leukocytes and macrophages that overproduce IL1, IL6, TNF and other proinflammatory cytokines and which has been associated with increased risk for endometrial cancers (66). Expression profiling of human ovarian endometriotic tissue showed high overall levels of NCOA1 and ER␤ as well as an increased abundance of NCOA1-and ER␤-stained cells (67,68). More recently, increased levels of ER␣ as well as NCOA1 and NCOA3 in endometriotic tissue have been described (69).…”

Section: Ncoas and Estrogen Receptors (Er␣ And Er␤)mentioning

confidence: 98%

Minireview: Nuclear Receptor Coregulators of the p160 Family: Insights into Inflammation and Metabolism

Rollins

Coppo

Rogatsky

2015

Molecular Endocrinology

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Nuclear receptor coactivators (NCOAs) are multifunctional transcriptional coregulators for a growing number of signal-activated transcription factors. The members of the p160 family (NCOA1/2/3) are increasingly recognized as essential and nonredundant players in a number of physiological processes. In particular, accumulating evidence points to the pivotal roles that these coregulators play in inflammatory and metabolic pathways, both under homeostasis and in disease. Given that chronic inflammation of metabolic tissues ("metainflammation") is a driving force for the widespread epidemic of obesity, insulin resistance, cardiovascular disease, and associated comorbidities, deciphering the role of NCOAs in "normal" vs "pathological" inflammation and in metabolic processes is indeed a subject of extreme biomedical importance. Here, we review the evolving and, at times, contradictory, literature on the pleiotropic functions of NCOA1/2/3 in inflammation and metabolism as related to nuclear receptor actions and beyond. We then briefly discuss the potential utility of NCOAs as predictive markers for disease and/or possible therapeutic targets once a better understanding of their molecular and physiological actions is achieved.

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Hormonal treatments for endometriosis: The endocrine background

Vannuccini

Clemenza

Rossi

et al. 2021

Rev Endocr Metab Disord

109

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Endometriosis is a benign uterine disorder characterized by menstrual pain and infertility, deeply affecting women’s health. It is a chronic disease and requires a long term management. Hormonal drugs are currently the most used for the medical treatment and are based on the endocrine pathogenetic aspects. Estrogen-dependency and progesterone-resistance are the key events which cause the ectopic implantation of endometrial cells, decreasing apoptosis and increasing oxidative stress, inflammation and neuroangiogenesis. Endometriotic cells express AMH, TGF-related growth factors (inhibin, activin, follistatin) CRH and stress related peptides. Endocrine and inflammatory changes explain pain and infertility, and the systemic comorbidities described in these patients, such as autoimmune (thyroiditis, arthritis, allergies), inflammatory (gastrointestinal/urinary diseases) and mental health disorders.The hormonal treatment of endometriosis aims to block of menstruation through an inhibition of hypothalamus-pituitary-ovary axis or by causing a pseudodecidualization with consequent amenorrhea, impairing the progression of endometriotic implants. GnRH agonists and antagonists are effective on endometriosis by acting on pituitary-ovarian function. Progestins are mostly used for long term treatments (dienogest, NETA, MPA) and act on multiple sites of action. Combined oral contraceptives are also used for reducing endometriosis symptoms by inhibiting ovarian function. Clinical trials are currently going on selective progesterone receptor modulators, selective estrogen receptor modulators and aromatase inhibitors. Nowadays, all these hormonal drugs are considered the first-line treatment for women with endometriosis to improve their symptoms, to postpone surgery or to prevent post-surgical disease recurrence. This review aims to provide a comprehensive state-of-the-art on the current and future hormonal treatments for endometriosis, exploring the endocrine background of the disease.

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Expression patterns of the steroid receptor coactivator family in human ovarian endometriosis

Cited by 15 publications

References 27 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

Minireview: Nuclear Receptor Coregulators of the p160 Family: Insights into Inflammation and Metabolism

Hormonal treatments for endometriosis: The endocrine background

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