An assessment of the multifactorial profile of steroid-metabolizing enzymes and steroid receptors in the eutopic endometrium during moderate to severe ovarian endometriosis

Background Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions, presumably because the relative effects of type of endometriosis, fertility history and menstrual cycle phases on the measured varia...

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Published inReproductive biology and endocrinology Vol. 17; no. 1; pp. 111 - 16
Main Authors Anupa, G., Sharma, Jai Bhagwan, Roy, Kallol K., Sengupta, Jayasree, Ghosh, Debabrata
Format Journal Article
LanguageEnglish
Published London BioMed Central 26.12.2019
BioMed Central Ltd
BMC
Subjects
17-Hydroxysteroid Dehydrogenases - analysis
17-Hydroxysteroid Dehydrogenases - genetics
Adolescent
Adult
Aromatase
Aromatase - analysis
Aromatase - genetics
Comparative analysis
Cytochrome P-450
Endocrinology
Endometriosis
Endometriosis - metabolism
Endometrium
Endometrium - chemistry
Endometrium - metabolism
Enzymes
Estradiol - analysis
Female
Fertility
Fibroblasts
Gene Expression
Genes
Gonadal Steroid Hormones - metabolism
Humans
Hyperestrogenism
Immunoblotting
Infertility
Infertility, Female - metabolism
Laboratories
Medicine
Medicine & Public Health
Menstrual Cycle
Menstruation
Messenger RNA
Metabolism
Obstetrics
Ovarian Diseases - metabolism
Patients
Physiological aspects
Physiology
Progesterone
Progesterone - analysis
Proteins
Receptors, Estrogen - analysis
Receptors, Progesterone - analysis
Receptors, Steroid - genetics
Receptors, Steroid - metabolism
Reproductive Medicine
RNA
Sex hormones
Steroid hormone receptors
Steroid hormones
Steroid receptors
Studies
Tuberculosis
Young Adult
United States > US
Endometriosis
Menstrual cycle
Aromatase
Infertility
Endometrium
Steroid receptors
Online AccessGet full text
ISSN1477-7827
1477-7827
DOI10.1186/s12958-019-0553-0

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Abstract Background Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions, presumably because the relative effects of type of endometriosis, fertility history and menstrual cycle phases on the measured variables were not considered. In the present study, endometrial mRNA and protein levels of several effectors of steroid biosynthesis and action in patients with stage III-IV ovarian endometriosis (OE) with known fertility and menstrual cycle histories were compared with the levels in control endometrium to test this concept. Methods Endometrial samples were collected from patients without endometriosis ( n  = 32) or OE stages III-IV ( n  = 52) with known fertility and cycle histories. qRT-PCR and immunoblotting experiments were performed to measure levels of NR5A1, STAR, CYP19A1, HSD17Bs, ESRs and PGR transcripts and proteins, respectively. Tissue concentrations of steroids (P4, T, E1 and E2) were measured using ELISAs. Results The levels of expression of aromatase and ERβ were lower ( P  < 0.0001) and 17β-HSD1 ( P  < 0.0001) and PRA ( P  < 0.01) were higher in OE endometrium. Lower aromatase levels and higher 17β-HSD1 levels were detected in fertile (aromatase: P  < 0.05; 17β-HSD1: P  < 0.0001) and infertile (aromatase: P  < 0.0001; 17β-HSD1: P  < 0.0001) OE endometrium than in the matched control tissues. Both proliferative (PP) and secretory (SP) phase OE samples expressed aromatase ( P  < 0.0001) and ERβ (PP: P  < 0.001; SP: P  < 0.01) at lower levels and 17β-HSD1 ( P  < 0.0001) and PRA (PP: P  < 0.01; SP: P  < 0.0001) at higher levels than matched controls. Higher 17β-HSD1 ( P  < 0.01) and E2 ( P  < 0.05) levels and a lower ( P  < 0.01) PRB/PRA ratio was observed in infertile secretory phase OE endometrium than in control. Conclusions We report that dysregulated expression of 17β-HSD1 and PGR resulting in hyperestrogenism and progesterone resistance during the secretory phase of the menstrual cycle, rather than an anomaly in aromatase expression, was the hallmark of eutopic endometrium from infertile OE patients. Furthermore, the results provide proof of concept that the fertility and menstrual cycle histories exerted relatively different effects on steroid physiology in the endometrium from OE patients compared with the control subjects.
AbstractList Abstract Background Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions, presumably because the relative effects of type of endometriosis, fertility history and menstrual cycle phases on the measured variables were not considered. In the present study, endometrial mRNA and protein levels of several effectors of steroid biosynthesis and action in patients with stage III-IV ovarian endometriosis (OE) with known fertility and menstrual cycle histories were compared with the levels in control endometrium to test this concept. Methods Endometrial samples were collected from patients without endometriosis (n = 32) or OE stages III-IV (n = 52) with known fertility and cycle histories. qRT-PCR and immunoblotting experiments were performed to measure levels of NR5A1, STAR, CYP19A1, HSD17Bs, ESRs and PGR transcripts and proteins, respectively. Tissue concentrations of steroids (P4, T, E1 and E2) were measured using ELISAs. Results The levels of expression of aromatase and ERβ were lower (P < 0.0001) and 17β-HSD1 (P < 0.0001) and PRA (P < 0.01) were higher in OE endometrium. Lower aromatase levels and higher 17β-HSD1 levels were detected in fertile (aromatase: P < 0.05; 17β-HSD1: P < 0.0001) and infertile (aromatase: P < 0.0001; 17β-HSD1: P < 0.0001) OE endometrium than in the matched control tissues. Both proliferative (PP) and secretory (SP) phase OE samples expressed aromatase (P < 0.0001) and ERβ (PP: P < 0.001; SP: P < 0.01) at lower levels and 17β-HSD1 (P < 0.0001) and PRA (PP: P < 0.01; SP: P < 0.0001) at higher levels than matched controls. Higher 17β-HSD1 (P < 0.01) and E2 (P < 0.05) levels and a lower (P < 0.01) PRB/PRA ratio was observed in infertile secretory phase OE endometrium than in control. Conclusions We report that dysregulated expression of 17β-HSD1 and PGR resulting in hyperestrogenism and progesterone resistance during the secretory phase of the menstrual cycle, rather than an anomaly in aromatase expression, was the hallmark of eutopic endometrium from infertile OE patients. Furthermore, the results provide proof of concept that the fertility and menstrual cycle histories exerted relatively different effects on steroid physiology in the endometrium from OE patients compared with the control subjects.
Background Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions, presumably because the relative effects of type of endometriosis, fertility history and menstrual cycle phases on the measured variables were not considered. In the present study, endometrial mRNA and protein levels of several effectors of steroid biosynthesis and action in patients with stage III-IV ovarian endometriosis (OE) with known fertility and menstrual cycle histories were compared with the levels in control endometrium to test this concept. Methods Endometrial samples were collected from patients without endometriosis ( n  = 32) or OE stages III-IV ( n  = 52) with known fertility and cycle histories. qRT-PCR and immunoblotting experiments were performed to measure levels of NR5A1, STAR, CYP19A1, HSD17Bs, ESRs and PGR transcripts and proteins, respectively. Tissue concentrations of steroids (P4, T, E1 and E2) were measured using ELISAs. Results The levels of expression of aromatase and ERβ were lower ( P  < 0.0001) and 17β-HSD1 ( P  < 0.0001) and PRA ( P  < 0.01) were higher in OE endometrium. Lower aromatase levels and higher 17β-HSD1 levels were detected in fertile (aromatase: P  < 0.05; 17β-HSD1: P  < 0.0001) and infertile (aromatase: P  < 0.0001; 17β-HSD1: P  < 0.0001) OE endometrium than in the matched control tissues. Both proliferative (PP) and secretory (SP) phase OE samples expressed aromatase ( P  < 0.0001) and ERβ (PP: P  < 0.001; SP: P  < 0.01) at lower levels and 17β-HSD1 ( P  < 0.0001) and PRA (PP: P  < 0.01; SP: P  < 0.0001) at higher levels than matched controls. Higher 17β-HSD1 ( P  < 0.01) and E2 ( P  < 0.05) levels and a lower ( P  < 0.01) PRB/PRA ratio was observed in infertile secretory phase OE endometrium than in control. Conclusions We report that dysregulated expression of 17β-HSD1 and PGR resulting in hyperestrogenism and progesterone resistance during the secretory phase of the menstrual cycle, rather than an anomaly in aromatase expression, was the hallmark of eutopic endometrium from infertile OE patients. Furthermore, the results provide proof of concept that the fertility and menstrual cycle histories exerted relatively different effects on steroid physiology in the endometrium from OE patients compared with the control subjects.
Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions, presumably because the relative effects of type of endometriosis, fertility history and menstrual cycle phases on the measured variables were not considered. In the present study, endometrial mRNA and protein levels of several effectors of steroid biosynthesis and action in patients with stage III-IV ovarian endometriosis (OE) with known fertility and menstrual cycle histories were compared with the levels in control endometrium to test this concept.BACKGROUNDPrevious studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions, presumably because the relative effects of type of endometriosis, fertility history and menstrual cycle phases on the measured variables were not considered. In the present study, endometrial mRNA and protein levels of several effectors of steroid biosynthesis and action in patients with stage III-IV ovarian endometriosis (OE) with known fertility and menstrual cycle histories were compared with the levels in control endometrium to test this concept.Endometrial samples were collected from patients without endometriosis (n = 32) or OE stages III-IV (n = 52) with known fertility and cycle histories. qRT-PCR and immunoblotting experiments were performed to measure levels of NR5A1, STAR, CYP19A1, HSD17Bs, ESRs and PGR transcripts and proteins, respectively. Tissue concentrations of steroids (P4, T, E1 and E2) were measured using ELISAs.METHODSEndometrial samples were collected from patients without endometriosis (n = 32) or OE stages III-IV (n = 52) with known fertility and cycle histories. qRT-PCR and immunoblotting experiments were performed to measure levels of NR5A1, STAR, CYP19A1, HSD17Bs, ESRs and PGR transcripts and proteins, respectively. Tissue concentrations of steroids (P4, T, E1 and E2) were measured using ELISAs.The levels of expression of aromatase and ERβ were lower (P < 0.0001) and 17β-HSD1 (P < 0.0001) and PRA (P < 0.01) were higher in OE endometrium. Lower aromatase levels and higher 17β-HSD1 levels were detected in fertile (aromatase: P < 0.05; 17β-HSD1: P < 0.0001) and infertile (aromatase: P < 0.0001; 17β-HSD1: P < 0.0001) OE endometrium than in the matched control tissues. Both proliferative (PP) and secretory (SP) phase OE samples expressed aromatase (P < 0.0001) and ERβ (PP: P < 0.001; SP: P < 0.01) at lower levels and 17β-HSD1 (P < 0.0001) and PRA (PP: P < 0.01; SP: P < 0.0001) at higher levels than matched controls. Higher 17β-HSD1 (P < 0.01) and E2 (P < 0.05) levels and a lower (P < 0.01) PRB/PRA ratio was observed in infertile secretory phase OE endometrium than in control.RESULTSThe levels of expression of aromatase and ERβ were lower (P < 0.0001) and 17β-HSD1 (P < 0.0001) and PRA (P < 0.01) were higher in OE endometrium. Lower aromatase levels and higher 17β-HSD1 levels were detected in fertile (aromatase: P < 0.05; 17β-HSD1: P < 0.0001) and infertile (aromatase: P < 0.0001; 17β-HSD1: P < 0.0001) OE endometrium than in the matched control tissues. Both proliferative (PP) and secretory (SP) phase OE samples expressed aromatase (P < 0.0001) and ERβ (PP: P < 0.001; SP: P < 0.01) at lower levels and 17β-HSD1 (P < 0.0001) and PRA (PP: P < 0.01; SP: P < 0.0001) at higher levels than matched controls. Higher 17β-HSD1 (P < 0.01) and E2 (P < 0.05) levels and a lower (P < 0.01) PRB/PRA ratio was observed in infertile secretory phase OE endometrium than in control.We report that dysregulated expression of 17β-HSD1 and PGR resulting in hyperestrogenism and progesterone resistance during the secretory phase of the menstrual cycle, rather than an anomaly in aromatase expression, was the hallmark of eutopic endometrium from infertile OE patients. Furthermore, the results provide proof of concept that the fertility and menstrual cycle histories exerted relatively different effects on steroid physiology in the endometrium from OE patients compared with the control subjects.CONCLUSIONSWe report that dysregulated expression of 17β-HSD1 and PGR resulting in hyperestrogenism and progesterone resistance during the secretory phase of the menstrual cycle, rather than an anomaly in aromatase expression, was the hallmark of eutopic endometrium from infertile OE patients. Furthermore, the results provide proof of concept that the fertility and menstrual cycle histories exerted relatively different effects on steroid physiology in the endometrium from OE patients compared with the control subjects.
Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions, presumably because the relative effects of type of endometriosis, fertility history and menstrual cycle phases on the measured variables were not considered. In the present study, endometrial mRNA and protein levels of several effectors of steroid biosynthesis and action in patients with stage III-IV ovarian endometriosis (OE) with known fertility and menstrual cycle histories were compared with the levels in control endometrium to test this concept. Endometrial samples were collected from patients without endometriosis (n = 32) or OE stages III-IV (n = 52) with known fertility and cycle histories. qRT-PCR and immunoblotting experiments were performed to measure levels of NR5A1, STAR, CYP19A1, HSD17Bs, ESRs and PGR transcripts and proteins, respectively. Tissue concentrations of steroids (P4, T, E1 and E2) were measured using ELISAs. The levels of expression of aromatase and ERβ were lower (P < 0.0001) and 17β-HSD1 (P < 0.0001) and PRA (P < 0.01) were higher in OE endometrium. Lower aromatase levels and higher 17β-HSD1 levels were detected in fertile (aromatase: P < 0.05; 17β-HSD1: P < 0.0001) and infertile (aromatase: P < 0.0001; 17β-HSD1: P < 0.0001) OE endometrium than in the matched control tissues. Both proliferative (PP) and secretory (SP) phase OE samples expressed aromatase (P < 0.0001) and ERβ (PP: P < 0.001; SP: P < 0.01) at lower levels and 17β-HSD1 (P < 0.0001) and PRA (PP: P < 0.01; SP: P < 0.0001) at higher levels than matched controls. Higher 17β-HSD1 (P < 0.01) and E2 (P < 0.05) levels and a lower (P < 0.01) PRB/PRA ratio was observed in infertile secretory phase OE endometrium than in control. We report that dysregulated expression of 17β-HSD1 and PGR resulting in hyperestrogenism and progesterone resistance during the secretory phase of the menstrual cycle, rather than an anomaly in aromatase expression, was the hallmark of eutopic endometrium from infertile OE patients. Furthermore, the results provide proof of concept that the fertility and menstrual cycle histories exerted relatively different effects on steroid physiology in the endometrium from OE patients compared with the control subjects.
Background Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions, presumably because the relative effects of type of endometriosis, fertility history and menstrual cycle phases on the measured variables were not considered. In the present study, endometrial mRNA and protein levels of several effectors of steroid biosynthesis and action in patients with stage III-IV ovarian endometriosis (OE) with known fertility and menstrual cycle histories were compared with the levels in control endometrium to test this concept. Methods Endometrial samples were collected from patients without endometriosis (n = 32) or OE stages III-IV (n = 52) with known fertility and cycle histories. qRT-PCR and immunoblotting experiments were performed to measure levels of NR5A1, STAR, CYP19A1, HSD17Bs, ESRs and PGR transcripts and proteins, respectively. Tissue concentrations of steroids (P4, T, E1 and E2) were measured using ELISAs. Results The levels of expression of aromatase and ER[beta] were lower (P < 0.0001) and 17[beta]-HSD1 (P < 0.0001) and PRA (P < 0.01) were higher in OE endometrium. Lower aromatase levels and higher 17[beta]-HSD1 levels were detected in fertile (aromatase: P < 0.05; 17[beta]-HSD1: P < 0.0001) and infertile (aromatase: P < 0.0001; 17[beta]-HSD1: P < 0.0001) OE endometrium than in the matched control tissues. Both proliferative (PP) and secretory (SP) phase OE samples expressed aromatase (P < 0.0001) and ER[beta] (PP: P < 0.001; SP: P < 0.01) at lower levels and 17[beta]-HSD1 (P < 0.0001) and PRA (PP: P < 0.01; SP: P < 0.0001) at higher levels than matched controls. Higher 17[beta]-HSD1 (P < 0.01) and E2 (P < 0.05) levels and a lower (P < 0.01) PRB/PRA ratio was observed in infertile secretory phase OE endometrium than in control. Conclusions We report that dysregulated expression of 17[beta]-HSD1 and PGR resulting in hyperestrogenism and progesterone resistance during the secretory phase of the menstrual cycle, rather than an anomaly in aromatase expression, was the hallmark of eutopic endometrium from infertile OE patients. Furthermore, the results provide proof of concept that the fertility and menstrual cycle histories exerted relatively different effects on steroid physiology in the endometrium from OE patients compared with the control subjects. Keywords: Aromatase, Endometriosis, Endometrium, Infertility, Menstrual cycle, Steroid receptors
Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions, presumably because the relative effects of type of endometriosis, fertility history and menstrual cycle phases on the measured variables were not considered. In the present study, endometrial mRNA and protein levels of several effectors of steroid biosynthesis and action in patients with stage III-IV ovarian endometriosis (OE) with known fertility and menstrual cycle histories were compared with the levels in control endometrium to test this concept. Endometrial samples were collected from patients without endometriosis (n = 32) or OE stages III-IV (n = 52) with known fertility and cycle histories. qRT-PCR and immunoblotting experiments were performed to measure levels of NR5A1, STAR, CYP19A1, HSD17Bs, ESRs and PGR transcripts and proteins, respectively. Tissue concentrations of steroids (P4, T, E1 and E2) were measured using ELISAs. The levels of expression of aromatase and ER[beta] were lower (P < 0.0001) and 17[beta]-HSD1 (P < 0.0001) and PRA (P < 0.01) were higher in OE endometrium. Lower aromatase levels and higher 17[beta]-HSD1 levels were detected in fertile (aromatase: P < 0.05; 17[beta]-HSD1: P < 0.0001) and infertile (aromatase: P < 0.0001; 17[beta]-HSD1: P < 0.0001) OE endometrium than in the matched control tissues. Both proliferative (PP) and secretory (SP) phase OE samples expressed aromatase (P < 0.0001) and ER[beta] (PP: P < 0.001; SP: P < 0.01) at lower levels and 17[beta]-HSD1 (P < 0.0001) and PRA (PP: P < 0.01; SP: P < 0.0001) at higher levels than matched controls. Higher 17[beta]-HSD1 (P < 0.01) and E2 (P < 0.05) levels and a lower (P < 0.01) PRB/PRA ratio was observed in infertile secretory phase OE endometrium than in control. We report that dysregulated expression of 17[beta]-HSD1 and PGR resulting in hyperestrogenism and progesterone resistance during the secretory phase of the menstrual cycle, rather than an anomaly in aromatase expression, was the hallmark of eutopic endometrium from infertile OE patients. Furthermore, the results provide proof of concept that the fertility and menstrual cycle histories exerted relatively different effects on steroid physiology in the endometrium from OE patients compared with the control subjects.
Background Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions, presumably because the relative effects of type of endometriosis, fertility history and menstrual cycle phases on the measured variables were not considered. In the present study, endometrial mRNA and protein levels of several effectors of steroid biosynthesis and action in patients with stage III-IV ovarian endometriosis (OE) with known fertility and menstrual cycle histories were compared with the levels in control endometrium to test this concept. Methods Endometrial samples were collected from patients without endometriosis (n = 32) or OE stages III-IV (n = 52) with known fertility and cycle histories. qRT-PCR and immunoblotting experiments were performed to measure levels of NR5A1, STAR, CYP19A1, HSD17Bs, ESRs and PGR transcripts and proteins, respectively. Tissue concentrations of steroids (P4, T, E1 and E2) were measured using ELISAs. Results The levels of expression of aromatase and ERβ were lower (P < 0.0001) and 17β-HSD1 (P < 0.0001) and PRA (P < 0.01) were higher in OE endometrium. Lower aromatase levels and higher 17β-HSD1 levels were detected in fertile (aromatase: P < 0.05; 17β-HSD1: P < 0.0001) and infertile (aromatase: P < 0.0001; 17β-HSD1: P < 0.0001) OE endometrium than in the matched control tissues. Both proliferative (PP) and secretory (SP) phase OE samples expressed aromatase (P < 0.0001) and ERβ (PP: P < 0.001; SP: P < 0.01) at lower levels and 17β-HSD1 (P < 0.0001) and PRA (PP: P < 0.01; SP: P < 0.0001) at higher levels than matched controls. Higher 17β-HSD1 (P < 0.01) and E2 (P < 0.05) levels and a lower (P < 0.01) PRB/PRA ratio was observed in infertile secretory phase OE endometrium than in control. Conclusions We report that dysregulated expression of 17β-HSD1 and PGR resulting in hyperestrogenism and progesterone resistance during the secretory phase of the menstrual cycle, rather than an anomaly in aromatase expression, was the hallmark of eutopic endometrium from infertile OE patients. Furthermore, the results provide proof of concept that the fertility and menstrual cycle histories exerted relatively different effects on steroid physiology in the endometrium from OE patients compared with the control subjects.
ArticleNumber 111
Audience Academic
Author Anupa, G.
Sharma, Jai Bhagwan
Sengupta, Jayasree
Ghosh, Debabrata
Roy, Kallol K.
Author_xml – sequence: 1
  givenname: G.
  surname: Anupa
  fullname: Anupa, G.
  organization: Department of Physiology, All India Institute of Medical Sciences, Department of Obstetrics and Gynecology, All India Institute of Medical Sciences
– sequence: 2
  givenname: Jai Bhagwan
  surname: Sharma
  fullname: Sharma, Jai Bhagwan
  organization: Department of Obstetrics and Gynecology, All India Institute of Medical Sciences
– sequence: 3
  givenname: Kallol K.
  surname: Roy
  fullname: Roy, Kallol K.
  organization: Department of Obstetrics and Gynecology, All India Institute of Medical Sciences
– sequence: 4
  givenname: Jayasree
  surname: Sengupta
  fullname: Sengupta, Jayasree
  organization: Department of Physiology, All India Institute of Medical Sciences
– sequence: 5
  givenname: Debabrata
  orcidid: 0000-0001-5699-4217
  surname: Ghosh
  fullname: Ghosh, Debabrata
  email: debabrata.ghosh1@gmail.com
  organization: Department of Physiology, All India Institute of Medical Sciences
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31878927$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Endometriosis
Menstrual cycle
Aromatase
Infertility
Endometrium
Steroid receptors
Language English
License Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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Snippet Background Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting...
Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting conclusions,...
Background Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly conflicting...
Abstract Background Previous studies of expression profiles of major endometrial effectors of steroid physiology in endometriosis have yielded markedly...
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StartPage 111
SubjectTerms 17-Hydroxysteroid Dehydrogenases - analysis
17-Hydroxysteroid Dehydrogenases - genetics
Adolescent
Adult
Aromatase
Aromatase - analysis
Aromatase - genetics
Comparative analysis
Cytochrome P-450
Endocrinology
Endometriosis
Endometriosis - metabolism
Endometrium
Endometrium - chemistry
Endometrium - metabolism
Enzymes
Estradiol - analysis
Female
Fertility
Fibroblasts
Gene Expression
Genes
Gonadal Steroid Hormones - metabolism
Humans
Hyperestrogenism
Immunoblotting
Infertility
Infertility, Female - metabolism
Laboratories
Medicine
Medicine & Public Health
Menstrual Cycle
Menstruation
Messenger RNA
Metabolism
Obstetrics
Ovarian Diseases - metabolism
Patients
Physiological aspects
Physiology
Progesterone
Progesterone - analysis
Proteins
Receptors, Estrogen - analysis
Receptors, Progesterone - analysis
Receptors, Steroid - genetics
Receptors, Steroid - metabolism
Reproductive Medicine
RNA
Sex hormones
Steroid hormone receptors
Steroid hormones
Steroid receptors
Studies
Tuberculosis
Young Adult
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Title An assessment of the multifactorial profile of steroid-metabolizing enzymes and steroid receptors in the eutopic endometrium during moderate to severe ovarian endometriosis
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