Expression of 17beta-hydroxysteroid dehydrogenase type 2 in pelvic endometriosis

Márcia M Carneiro, Márcia Mendonça Carneiro, Débora Martinho Morsch, Débora M Morsch, Morsch DM, Aroldo F. Camargos, Camargos AF, Poli Mara Spritzer, Poli M Spritzer, Fernando M. Reis
Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology · 2007 · vol. 23(4) , pp. 188–192 · doi:10.1080/09513590701200850 · PMID:17505937 · W2169417859
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This study found significantly higher 17beta-Hsd2 mRNA expression in endometriotic implants compared to eutopic endometrium from controls, refuting the hypothesis of deficient expression.

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Abstract

Lack of expression or a deficiency of 17beta-hydroxysteroid dehydrogenase type 2 (17beta-HSD2), a key enzyme in estradiol inactivation, could be involved in the pathophysiology of endometriosis. The aim of the present study was to evaluate expression of the gene (17beta-Hsd2) encoding 17beta-HSD2 in eutopic and ectopic endometrial tissues of women with endometriosis. Thirty-four infertile women were divided into a control group, without any clinical or laparoscopic evidence of endometriosis (n = 19), and a group with pelvic endometriosis (n = 15). Diagnosis was confirmed by histological examination of the endometriotic lesions. 17beta-Hsd2 mRNA expression was detected by reverse transcription-polymerase chain reaction in the control group (54% of the samples), in the eutopic endometrium of patients with endometriosis (83% of the specimens analyzed) and in all endometriotic lesions. The semi-quantitative analysis of 17beta-Hsd2 mRNA showed a significantly higher gene expression in the endometriotic implants compared with the intrauterine endometrium of the control group (p < 0.05). 17beta-HSD2 protein was localized to the glandular epithelium of both eutopic endometrium and endometriotic implants. The present results refute the hypothesis of lower or absent 17beta-HSD2 expression in pelvic endometriosis; therefore further studies are needed to assess other potential mechanisms leading to increased estrogenic activity within endometriotic implants.

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Condition tags

endometriosis

MeSH descriptors

17-Hydroxysteroid Dehydrogenases Endometriosis Gene Expression Regulation, Enzymologic Gene Expression Regulation, Enzymologic 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases Adult Adult Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium Estradiol Dehydrogenases Estradiol Dehydrogenases Female Female

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References (16)

Cited by (10)

SciLite annotations

chemicals 1
estradiol

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