Hormonal Therapy Deregulates Prostaglandin-Endoperoxidase Synthase 2 (PTGS2) Expression in Endometriotic Tissues

Piétro Santulli, Pietro Santulli, Bruno Borghese, Jean‐Christophe Noël, Jean-Christophe Noël, Isabelle Fayt, Vincent Anaf, Dominique de Ziegler, Frédéric Batteux, Frederic Batteux, Daniel Vaiman, Charles Chapron
The Journal of clinical endocrinology and metabolism · 2013 · vol. 99(3) , pp. 881–890 · doi:10.1210/jc.2013-2950 · PMID:24423291 · W2028348682
article OA: bronze CC0 ⤵ 39 in-corpus citations
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Endometriotic tissues exhibit significantly increased prostaglandin-endoperoxidase synthase 2 (PTGS2) expression, which is further elevated by hormonal therapy, suggesting a potential mechanism for treatment failure.

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Abstract

CONTEXT: Endometriosis is a common gynecologic condition characterized by an important inflammatory process mediated by the prostaglandin pathway. Oral contraceptives are the treatment of choice for symptomatic endometriotic women. However the effects of oral contraceptives use and prostaglandin pathway in endometriotic women are actually still unknown. OBJECTIVE: To investigate the expression of prostaglandin pathway key genes in endometriotic tissue, affected or not by hormonal therapy, as compared with healthy endometrial tissue. DESIGN: This was a comparative laboratory study. SETTING: This study was conducted in a tertiary-care university hospital. PATIENTS: Seventy-six women, with (n = 46) and without (n = 30) histologically proven endometriosis. MAIN OUTCOME MEASURES: Prostaglandin-endoperoxidase synthase (PTGS)1, PTGS2, prostaglandin E receptor (PTGER)1, PTGER2, PTGER3, and PTGER4 mRNA levels in endometrium of disease-free women and in eutopic and ectopic endometrium of endometriosis-affected women. PTGS2 expression was further investigated by immunohistochemistry, using specific monoclonal antibodies. PTGS2 expression was analyzed at mRNA and protein levels and correlated with taking hormonal treatment. RESULTS: PTGS2 expression was significantly increased in eutopic and ectopic endometrium as compared with healthy tissue (induction of 9.6- and 6.3-fold, respectively; P = .001). PTGS2 immunoreactivity increased gradually from normal endometrium to eutopic and ectopic endometrium (h-score of 96.7 ± 55.0, 128.3 ± 66.1, and 226.7 ± 62.6, respectively, P < .001). PTGER2, PTGER3, and PTGER4 expression increased significantly and gradually from normal to eutopic and ectopic endometrium, whereas PTGER1 remained unchanged. Patients under hormonal treatment had a higher PTGS2 expression at transcriptional and protein levels as compared with those without treatment (P = .002 and P = .025, respectively). CONCLUSIONS: Prostaglandin pathway is strongly deregulated in eutopic and ectopic endometrium of women suffering from endometriosis for the benefit of an increased PTGS2 expression. We show for the first time that hormonal treatment appears to enhance even more PTGS2 expression. These results contribute to explain why medical treatment could fail to control endometriosis progression.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Contraceptives, Oral, Hormonal Cyclooxygenase 2 Endometriosis Adult Case-Control Studies Contraceptives, Oral, Hormonal Contraceptives, Oral, Hormonal Cyclooxygenase 1 Cyclooxygenase 1 Cyclooxygenase 1 Cyclooxygenase 2 Cyclooxygenase 2 Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Gene Expression Regulation, Enzymologic Gene Expression Regulation, Enzymologic

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