Effects of steroid hormone on estrogen sulfotransferase and on steroid sulfatase expression in endometriosis tissue and stromal cells
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This study investigated the impact of steroid hormones on estrogen sulfotransferase and steroid sulfatase expression within endometriosis tissue and its associated stromal cells.
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Abstract
Endometriosis is an estrogen-dependent disease that afflicts about 10% of women in their reproductive age, causing severe pain and infertility. The potential roles of female steroid hormones in modulating key estrogen-metabolizing enzymes, steroid sulfatase (STS) and estrogen sulfotransferase (SULT1E1), were investigated. The expression of STS and SULT1E1 mRNA in biopsy samples (n=78) of superficial and deep endometriotic lesions, eutopic endometrium of women with endometriosis and endometrium from control patients were compared according to the menstrual cycle phase. Increased STS gene expression was detected in superficial and deep-infiltrating lesions and a reduced SULT1E1 expression was also observed in the eutopic endometrium relative to the superficial lesions. Additionally, a significantly positive correlation was detected between STS and SULT1E1 mRNA expression levels in biopsy specimens collected from the endometriosis patients, and not in control individuals. The actions of female steroid hormones on SULT1E1 and STS expression were evidenced in endometriosis, revealed by increased expression levels in the luteal phase of the cycle. There was an increased STS expression in primary eutopic and ectopic endometrial stromal cells treated with estradiol and progesterone (representative of the luteal phase, n=3). Although an increased STS mRNA expression was observed in hormone-induced endometrial stromal cells in vitro, no difference could be detected between the hormone treatment groups in estradiol formation from estradiol sulfate measured by LC-MS-MS. Interestingly, a greater expression of STS was observed in stromal cells from eutopic endometrium with an agreement in estradiol formation originated from estradiol sulfate. The differential regulation of STS and SULT1E1 could provide insights for novel studies of the therapeutic use of STS inhibitors.
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Cited by (15)
- Etiologies of endometriosis and model systems: is there a risk of a tunnel vision? 2025
- Higher Oxidative Stress in Endometriotic Lesions Upregulates Senescence-Associated p16ink4a and β-Galactosidase in Stromal Cells 2023
- Is intracrinology of endometriosis relevant in clinical practice? A systematic review on estrogen metabolism 2022
- Integrating Network Pharmacology and Experimental Validation Deciphers the Mechanism of Guizhi Fuling Wan against Adenomyosis 2021
- Clinical characteristics of perineal endometriosis: A case series 2021
- Integrating Network Pharmacology and Experimental Validation Deciphers the Mechanism of Guizhi Fuling Wan against Adenomyosis 2021
- An assessment of the multifactorial profile of steroid-metabolizing enzymes and steroid receptors in the eutopic endometrium during moderate to severe ovarian endometriosis 2019
- An assessment of the multifactorial profile of steroid-metabolizing enzymes and steroid receptors in the eutopic endometrium during moderate to severe ovarian endometriosis 2019
- Comparative analysis of eutopic endometrium from women with and without endometriosis 2018
- Endometrial Intracrinology: Oestrogens, Androgens and Endometrial Disorders 2018
- Enhanced UGT1A1 Gene and Protein Expression in Endometriotic Lesions 2018
- Endometrial Intracrinology: Oestrogens, Androgens and Endometrial Disorders 2018
- SULFATION PATHWAYS: Contribution of intracrine oestrogens to the aetiology of endometriosis 2018
- Increased expression of <i>CYP1A1</i> and <i>CYP1B1</i> in ovarian/peritoneal endometriotic lesions 2016
- Is cytochrome P450 3A4 regulated by menstrual cycle hormones in control endometrium and endometriosis? 2016
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