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Elevated expression of CYP1A1 and y-SYNUCLEIN in human ectopic (ovarian) endometriosis compared with eutopic endometrium.

Research output: Contribution to journalJournal article


Journal publication date11/2008
JournalMolecular Human Reproduction
Number of pages9
Original languageEnglish


Endometriosis is a debilitating disease in which apoptotic, genetic, immunological, angiogenic and environmental factors have been implicated. Endocrine-disrupting agents (e.g. dioxins) might be involved. Dioxins, via the arylhydrocarbon receptor (AhR), induce estrogen-metabolizing enzymes CYP1A1 and CYP1B1. Elevated expression of -SYNUCLEIN (-SYN) has been associated with hormone-related conditions. Tissue sets consisting of eutopic and ectopic (ovarian) endometrium from patients with stage 3 or 4 endometriosis were obtained. Following RNA extraction and reverse transcription, quantitative real-time reverse transcriptase–polymerase chain reaction was performed for anti-apoptotic B-cell leukaemia/lymphoma 2 (BCL-2), CYP1A1, CYP1B1, estrogen receptor (ER), ERβ and -SYN. Immunohistochemical analyses for -syn, ER, ERβ and CYP1A1 were also conducted. A 3–9-fold increase in intra-individual expression of CYP1A1 in ectopic (ovarian) endometrium compared with eutopic tissue was observed; immunohistochemical analyses pointed to CYP1A1 being localized to the glandular epithelium. This intra-individual expression profile was not observed for CYP1B1 or BCL-2. However, a 5–53-fold intra-individual increase in -SYN expression was also demonstrated in six of nine tissue sets (a further two showed an increase that was not considered significant) when comparing ectopic to eutopic endometrium; -syn positivity was associated with endothelial cells. An elevation in ERβ was also noted when comparing ectopic to eutopic endometrium; with regard to ER, this was inconsistent. These results suggest an up-regulation of dioxin-inducible CYP1A1 and -SYN occurs in endometriosis. Whether -syn may be a novel diagnostic marker for endometriosis remains to be ascertained.