Estrogen metabolizing enzymes in endometrium and endometriosis

H Dassen, Chamindie Punyadeera, C Punyadeera, Rick Kamps, R Kamps, Bert Delvoux, B Delvoux, Anne Van Langendonckt, A Van Langendonckt, Jacques Donnez, J Donnez, Bettina Husen, B Husen, H Thole, H. Thöle, G.A.J. Dunselman, G Dunselman, Patrick G. Groothuis, P Groothuis
Human Reproduction · 2007 · vol. 22(12) , pp. 3148–3158 · doi:10.1093/humrep/dem310 · PMID:17921479 · W2117221582
article OA: closed CC0 ⤵ 90 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found that endometriosis lesions have an imbalance favoring estradiol production due to altered expression of estrogen metabolizing enzymes compared to normal endometrium.

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Abstract

BACKGROUND: Estradiol (E(2)) is an important promoter of the growth of both eutopic and ectopic endometrium. The findings with regard to the expression and activity of steroidogenic enzymes in endometrium of controls, in endometrium of endometriosis patients and in endometriotic lesions are not consistent. METHODS: In this study, we have looked at the mRNA expression and protein levels of a range of steroidogenic enzymes [aromatase, 17beta-hydroxysteroid dehydrogenases (17beta-HSD) type 1, 2 and 4, estrogen sulfotransferase (EST) and steroid sulfatase (STS)] in eutopic and ectopic endometrium of patients (n = 14) with deep-infiltrative endometriosis as well as in disease-free endometrium (n = 48) using real-time PCR and immunocytochemistry. In addition, we evaluated their menstrual cycle-related expression patterns, and investigated their steroid responsiveness in explant cultures. RESULTS: Aromatase and 17beta-HSD type 1 mRNA levels were extremely low in normal human endometrium, while mRNAs for types 2 and 4 17beta-HSD, EST and STS were readily detectable. Only 17beta-HSD type 2 and EST genes showed sensitivity to progesterone in normal endometrium. Types 1 and 2 17beta-HSD and STS protein was detected in normal endometrium using new polyclonal antibodies. CONCLUSIONS: In endometriosis lesions, the balance is tilted in favor of enzymes producing E(2). This is due to a suppression of types 2 and 4 17beta-HSD, and an increased expression of aromatase and type 1 17beta-HSD in ectopic endometrium.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometrium Estrogens 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases Adult Animals Antibody Specificity Aromatase Aromatase Aromatase Endometriosis Endometrium Estrogens Estrogens Female Gene Expression Regulation, Enzymologic Humans

Citation neighborhood

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References (68)

Cited by (50)

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License: CC0 · commercial use OK