HSD3B2, HSD17B1, HSD17B2, ESR1, ESR2 and AR expression in infertile women with endometriosis

Osiński, Maciej; Wirstlein, Przemysław; Wender-Ożegowska, Ewa; Mikołajczyk, Mateusz; Jagodzińśki, Paweł P.; Szczepańska, Magdalena

doi:10.5603/gp.a2018.0022

Cited by 25 publications

(19 citation statements)

References 30 publications

(55 reference statements)

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“…These GWAS results are not surprising since the symptoms of endometriosis are modulated by ovarian sex steroids; early age at menarche is a risk factor for development of endometriosis, suggesting increased exposure to estrogen may incur increased risk of disease (26). Endometriosis lesions aberrantly express a number of steroidogenic enzymes including aromatase and 17β-hydroxysteriod dehydrogenase (17β-HSD), this results in increased synthesis and decreased metabolism of estrogen (27)(28)(29) such that local levels remain high. Estrogen signaling modulates a large number of down-stream disease processes within endometriosis lesions, which are reviewed in Yilmaz and Bulun (30), Liang et al (31), and Rizner (32).…”

Section: Etiology and Natural Historymentioning

confidence: 97%

Endometriosis-Associated Macrophages: Origin, Phenotype, and Function

2020

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Endometriosis is a complex, heterogeneous, chronic inflammatory condition impacting ∼176 million women worldwide. It is associated with chronic pelvic pain, infertility, and fatigue, and has a substantial impact on health-related quality of life. Endometriosis is defined by the growth of endometrial-like tissue outside the uterus, typically on the lining of the pelvic cavity and ovaries (known as "lesions"). Macrophages are complex cells at the center of this enigmatic condition; they are critical for the growth, development, vascularization, and innervation of lesions as well as generation of pain symptoms. In health, tissue-resident macrophages are seeded during early embryonic life are vital for development and homeostasis of tissues. In the adult, under inflammatory challenge, monocytes are recruited from the blood and differentiate into macrophages in tissues where they fulfill functions, such as fighting infection and repairing wounds. The interplay between tissue-resident and recruited macrophages is now at the forefront of macrophage research due to their differential roles in inflammatory disorders. In some cancers, tumor-associated macrophages (TAMs) are comprised of tissue-resident macrophages and recruited inflammatory monocytes that differentiate into macrophages within the tumor. These macrophages of different origins play differential roles in disease progression. Herein, we review the complexities of macrophage dynamics in health and disease and explore the paradigm that under disease-modified conditions, macrophages that normally maintain homeostasis become modified such that they promote disease. We also interrogate the evidence to support the existence of multiple phenotypic populations and origins of macrophages in endometriosis and how this could be exploited for therapy.

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Section: Etiology and Natural Historymentioning

confidence: 97%

Endometriosis-Associated Macrophages: Origin, Phenotype, and Function

2020

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“…The Δ 5 to Δ 4 isomerization of androstenes (DHEA, androstenediol -A5- and 17αA5) and pregnenes (P5, 17OHP5) is catalyzed by 3βHSD1, which is the peripheral counterpart of ovarian 3βHSD2. Also 3βHSD2, whose expression was initially considered to be restricted to endocrine tissues, is detected peripherally in recent reports (Stoffel-Wagner, 2001 ; Tsai et al, 2001 ; Attar et al, 2009 ; Huhtinen et al, 2014 ; Osinski et al, 2018 ). Due to the high concentration of DHEA (both in blood and tissues), its conversion to A4 by 3βHSDs is relevant to the formation of downstream androgens and of estrogens.…”

Section: From Ovarian Estrogen Synthesis To Intracrinologymentioning

confidence: 98%

Intracrine Regulation of Estrogen and Other Sex Steroid Levels in Endometrium and Non-gynecological Tissues; Pathology, Physiology, and Drug Discovery

et al. 2018

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Our understanding of the intracrine (or local) regulation of estrogen and other steroid synthesis and degradation expanded in the last decades, also thanks to recent technological advances in chromatography mass-spectrometry. Estrogen responsive tissues and organs are not passive receivers of the pool of steroids present in the blood but they can actively modify the intra-tissue steroid concentrations. This allows fine-tuning the exposure of responsive tissues and organs to estrogens and other steroids in order to best respond to the physiological needs of each specific organ. Deviations in such intracrine control can lead to unbalanced steroid hormone exposure and disturbances. Through a systematic bibliographic search on the expression of the intracrine enzymes in various tissues, this review gives an up-to-date view of the intracrine estrogen metabolisms, and to a lesser extent that of progestogens and androgens, in the lower female genital tract, including the physiological control of endometrial functions, receptivity, menopausal status and related pathological conditions. An overview of the intracrine regulation in extra gynecological tissues such as the lungs, gastrointestinal tract, brain, colon and bone is given. Current therapeutic approaches aimed at interfering with these metabolisms and future perspectives are discussed.

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“…Since E2′s effects are primarily enacted through ESR1 and ESR2, their expression levels are important in the assessment of E2 action in endometriosis. ESR1 levels are reportedly increased in the secretory phase endometrium of women with endometriosis compared to controls [172,173], which may lead to increased estrogenic activity and proliferation, compromising normal uterine function. ESR2 expression is unchanged in eutopic endometrium from women with endometriosis [173] although one study reported increased ESR2/ESR1 ratio in endometriosis-affected endometrium [174].…”

Section: Dysregulation Of Progesterone and Estrogen Signaling In Ementioning

confidence: 99%

“…ESR1 levels are reportedly increased in the secretory phase endometrium of women with endometriosis compared to controls [172,173], which may lead to increased estrogenic activity and proliferation, compromising normal uterine function. ESR2 expression is unchanged in eutopic endometrium from women with endometriosis [173] although one study reported increased ESR2/ESR1 ratio in endometriosis-affected endometrium [174]. The role of ESR2 in normal uterine physiology is not clear since ESR2 knockout mice have been reported to have no overt uterine defect [76,77]; however, one study implicated ESR2 in control of proliferation through epidermal growth factor (EGF) signaling [78].…”

Section: Dysregulation Of Progesterone and Estrogen Signaling In Ementioning

confidence: 99%

Progesterone and Estrogen Signaling in the Endometrium: What Goes Wrong in Endometriosis?

Marquardt

Kim

Shin

et al. 2019

IJMS

285

203

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In the healthy endometrium, progesterone and estrogen signaling coordinate in a tightly regulated, dynamic interplay to drive a normal menstrual cycle and promote an embryo-receptive state to allow implantation during the window of receptivity. It is well-established that progesterone and estrogen act primarily through their cognate receptors to set off cascades of signaling pathways and enact large-scale gene expression programs. In endometriosis, when endometrial tissue grows outside the uterine cavity, progesterone and estrogen signaling are disrupted, commonly resulting in progesterone resistance and estrogen dominance. This hormone imbalance leads to heightened inflammation and may also increase the pelvic pain of the disease and decrease endometrial receptivity to embryo implantation. This review focuses on the molecular mechanisms governing progesterone and estrogen signaling supporting endometrial function and how they become dysregulated in endometriosis. Understanding how these mechanisms contribute to the pelvic pain and infertility associated with endometriosis will open new avenues of targeted medical therapies to give relief to the millions of women suffering its effects.

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HSD3B2, HSD17B1, HSD17B2, ESR1, ESR2 and AR expression in infertile women with endometriosis

Abstract: Observed significant increase in HSD3B2 and ESR1 transcripts in follicular eutopic endometrium from infer-tile women with endometriosis may be related to abnormal biological effect of E2 in endometrium, further affecting the development of human embryos.

Cited by 25 publications

References 30 publications

Endometriosis-Associated Macrophages: Origin, Phenotype, and Function

Endometriosis-Associated Macrophages: Origin, Phenotype, and Function

Intracrine Regulation of Estrogen and Other Sex Steroid Levels in Endometrium and Non-gynecological Tissues; Pathology, Physiology, and Drug Discovery

Progesterone and Estrogen Signaling in the Endometrium: What Goes Wrong in Endometriosis?

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