Regulation of aromatase P450 expression in endometriotic and endometrial stromal cells by CCAAT/enhancer binding proteins (C/EBPs): decreased C/EBPbeta in endometriosis is associated with overexpression of aromatase.
The results point to the higher (2.45-fold) difference in aromatase expression in patients with endometriosis stage III-IV compared to controls and provide direct evidence that screening for eutopic endometrial aromatase expression in combination with clinical data could be of discriminative value in the prediction of estrogen-dependent diseases, independent from body mass index.
Androstenedione up-regulation of endometrial aromatase expression via local conversion to estrogen: potential relevance to the pathogenesis of endometriosis.
Endometriosis implants are characterized by unbalanced local oestrogen metabolism leading to hyperoestrogenism and aromatase up-regulation is one of main mechanism involved.
The estradiol concentration of the conditioned media and P450 aromatase mRNA expression in the endometriosis group were statistically significantly lower than that of the control group, irrespective of letrozole concentrations.
COX-2 mRNA level in unmethylated endometrium of the endometriosis group or the control group was 2.39-fold and 2.66-fold, respectively, higher than that in the methylated endometrium of the same group (P < 0.01).
Because overexpression of COX-2 has been demonstrated to be a master regulator in endometriosis progression, our data demonstrate the critical function of proinflammatory cytokines and the COUP-TFII regulatory gene network in the progression of endometriosis.
Aromatase expression was assessed by real-time RT-PCR in biopsied endometriotic tissues [peritoneal (n=19), ovarian (n=17) endometriosis and deep endometriotic nodules of the recto-vaginal septum (n=29)].
Consistent with these data, enzyme-linked immunosorbent assay showed that moderate to severe endometriosis was associated with markedly elevated levels of IL-10 in the peritoneal fluid.
A comparison of PR and AR mRNA levels in the pelvic peritoneum of the endometriosis and the nonendometriosis groups revealed no significant differences.
Specimens from ovarian endometrioma (OE), endometrium with endometriosis (EE), and normal endometrium (NE) were analyzed for PGC-1α and aromatase expression.
The molecular basis of progesterone resistance in endometriosis may be related to an overall reduction in the levels of progesterone receptors (PRs) and the lack of the PR isoform named progesterone receptor B (PR-B).
Oestrogen metabolism, including the expression pattern of aromatase and the regulation of 17beta-hydroxysteroid dehydrogenase type 2 is altered in the eutopic endometrium of women with endometriosis, adenomyosis, and/or leiomyomas compared to that in the eutopic endometrium of women without disease.
Together, these data suggest that KRAS, SIRT1 and BCL6 are coordinately over-expressed in eutopic endometrium of women with endometriosis and likely participate in the pathogenesis of endometriosis.
We examined stage-specific expression of aromatase, COX-2, ER, and PR isoform expression in eutopic endometrium, implants, peritoneum, and endometrioma samples from endometriosis patients.
IL-6 and IL-10 mRNA were expressed by nine and seven patients respectively in the endometriosis group compared with three and one patients in the control group; this difference was significant (P < 0.05).
This finding may be helpful in understanding infertility associated with endometriosis and reduced P450 aromatase activity in endometriotic granulosa cells.
The present study was conducted to determine the presence or absence of aromatase expression in peritoneal endometriotic implants and in the eutopic endometrium of women with endometriosis.