Absence of aromatase protein and mRNA expression in endometriosis

Abstract

Unlike previous studies, we observed no aromatase protein in any of the endometriosis types, and barely detectable aromatase mRNA expression, suggesting that locally produced aromatase (within endometriotic lesions) may be less implicated in endometriosis development than previously postulated. Potential factors responsible for these discrepancies are discussed.

P450Arom induction in isolated control endometrial cells by peritoneal fluid from women with endometriosis

“…The mRNA, protein, and/or activity of P 450 Arom have been shown in eutopic and/or ectopic endometria of women with endometriosis by several investigators using diverse techniques (4,17,20,21,23,33); recently, Colette et al (34) detected only low levels in ectopic endometrium. The cellular location of P 450 Arom is controversial because some investigators found it mainly in the glandular and superficial epithelia (4,35,36), others in the stromal cell compartment (4,13,14), or in both (22,37).…”

Effect of letrozole on estradiol production and P450 aromatase messenger RNA expression of cultured luteinized granulosa cells from women with and without endometriosis

“…However, there has been a large variation in the P450 aromatase mRNA expression in endometriotic tissue reported in published data (6,(20)(21)(22). Moreover, increased expression of P450 aromatase in endometriotic tissue has been recently challenged, as aromatase protein is undetectable in the endometriotic lesions and eutopic endometrium of women with endometriosis (23,24). Delvoux et al (24) believe a hyperestrogenic environment of endometriotic lesions is not caused by changes in the aromatase activity but rather is the result of increased reduction of estrone into estradiol and decreased oxidation of estradiol into estrone.…”

Pyrrolidine Dithiocarbamate Attenuates Nuclear Factor-ĸB Activation, Cyclooxygenase-2 Expression and Prostaglandin E₂ Production in Human Endometriotic Epithelial Cells

“…In addition, PGE 2 increases VEGF production, which may be involved in the establishment, maintenance and growth of endometriosis through the process of angiogenesis [19]. So even if some authors demonstrated the absence of aromatase protein in endometriosis [20], COX-2/PGE 2 may promote the pathophysiology and pathogenesis of endometriosis through multiple mechanisms. In the present study, we presented evidence that PDTC suppressed TNF-α-induced PGE 2 production by EECs.…”