Inhibition of type 1 17β-hydroxysteroid dehydrogenase impairs the synthesis of 17β-estradiol in endometriosis lesions

Bert Delvoux, Delvoux B, Thomas D’Hooghe, Thomas D'Hooghe, D'Hooghe T, Kyama C, Cleophas Kyama, Pasi Koskimies, Koskimies P, Hermans RJ, Rob Hermans, Rob J J Hermans, Gerard A Dunselman, Dunselman GA, Gerard A.J. Dunselman, Andrea Romano
The Journal of clinical endocrinology and metabolism · 2013 · vol. 99(1) , pp. 276–284 · doi:10.1210/jc.2013-2851 · PMID:24187399 · W2059133635
Lab / animal OA: bronze CC0 ⤵ 24 in-corpus citations
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This study found that type 1 17β-hydroxysteroid dehydrogenase is upregulated in endometriosis lesions, leading to increased 17β-estradiol synthesis, and its inhibition restored normal estrogen metabolism.

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Abstract

CONTEXT: Endometriosis affects 10% of the women before menopause and has important personal, professional, and societal economic burdens. Because current medical treatments are aimed at reducing the symptoms only, novel therapeutic targets should be identified. Endometriosis is estrogen dependent and in some patients the endometriosis tissue is able to produce estrogens in an autocrine/paracrine manner. In a number of patients, this is the consequence of the high local activity of the 17β-hydroxysteroid-dehydrogenases (17β-HSDs), enzymes able to generate active estrogens from precursors with low activity. OBJECTIVE: The objective of the study was to identify the 17β-HSD(s) responsible for the high local generation of estrogens in endometriosis and test the possibility to inhibit these enzymes for therapeutic purposes. DESIGN: The expression of different 17β-HSDs involved in the estrogen metabolism was assessed by real-time PCR in eutopic and ectopic tissue from endometriosis patients (n=14). These biopsies had previously confirmed unbalanced local 17β-HSD activity, which caused high estrogen generation. The possibility to block the synthesis of estrogens by one inhibitor specific for type 1 17β-HSD was assessed by HPLC in tissue lysates from endometriosis tissues (n=27). RESULTS: In all but one of the patients, a high type 1 17β-HSD level is associated with the unbalanced metabolism of estrogens, leading to higher estrogen synthesis in endometriosis than in the endometrium inside the uterus. Inhibition of type 1 17β-HSD restores to various extents, depending on the patient, the correct metabolism. In 19 of 27 patients analyzed (70%), the 17β-HSD type 1 inhibitor decreased the generation of 17β-estradiol by greater than 85%. CONCLUSIONS: Inhibition of 17β-HSD type 1 can be a potential future treatment option aimed at restoring the correct metabolic balance of estrogens in endometriosis patients with increased local 17β-HSD type 1 enzyme activity.

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Condition tags

endometriosis

MeSH descriptors

17-Hydroxysteroid Dehydrogenases Endometriosis Estradiol 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases Cells, Cultured Cells, Cultured Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium Endometrium Enzyme Inhibitors Enzyme Inhibitors Enzyme Inhibitors

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (43)

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