title: Expression of Ah receptor and dioxin-related genes in human uterine endometrium in women with or without endometriosis.
abstract: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been suggested as a possible etiologic factor for endometriosis, a condition in which endometrium-like tissues are present outside the uterus. The prevailing view pertaining to the origin of endometriotic cells is that they are from eutopic endometrial cells which regurgitate through fallopian tubes. In order to get insight into the possible involvement of TCDD in the pathogenesis of endometriosis, we suspected that TCDD may act differently on the endometrium with or without endometriosis. To address this, we examined the presence of messenger RNAs of arylhydrocarbon receptor (AhR), AhR nuclear translocator (Arnt) and two dioxin-responsive genes, cytochrome P-450 1B1 (CYP1B1) and downstream of tyrosine kinases (p62(dok)), in the endometrium of women with or without endometriosis using semi-quantitative reverse transcription-polymerase chain reaction. All the genes were expressed throughout the menstrual cycle. The expression level of p62(dok) was higher in the proliferative phase than in the secretory phase. In contrast, the expression levels of AhR, Arnt and CYP1B1 seemed to be constant during the cycle. In terms of the comparison between non-endometriosis and endometriosis group, the mRNA levels of AhR, Arnt, CYP1B1 and p62(dok) were essentially similar. Interestingly, AhR mRNA level was significantly lower in smokers than in non-smokers. Based on the regression analysis, significant linear and positive correlations were observed between AhR and Arnt mRNA levels, and between Arnt and p62(dok) mRNA levels. In summary, expression of AhR and dioxin-related genes in the endometrium did not differ in women with or without endometriosis.
authors.affiliation: Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Igarashi
authors.forename: U
authors.initials: U
authors.lastname: Osuga
authors.forename: O
authors.initials: O
authors.lastname: Tsutsumi
authors.forename: M
authors.initials: M
authors.lastname: Momoeda
authors.forename: K
authors.initials: K
authors.lastname: Ando
authors.forename: H
authors.initials: H
authors.lastname: Matsumi
authors.forename: Y
authors.initials: Y
authors.lastname: Takai
authors.forename: R
authors.initials: R
authors.lastname: Okagaki
authors.forename: H
authors.initials: H
authors.lastname: Hiroi
authors.forename: O
authors.initials: O
authors.lastname: Fujiwara
authors.forename: T
authors.initials: T
authors.lastname: Yano
authors.forename: Y
authors.initials: Y
authors.lastname: Taketani
mesh_terms: D000328:Adult; D001189:Aryl Hydrocarbon Hydroxylases; D051784:Aryl Hydrocarbon Receptor Nuclear Translocator; D065633:Cytochrome P-450 CYP1B1; D003577:Cytochrome P-450 Enzyme System / Q000235:genetics*; D004268:DNA-Binding Proteins; D004715:Endometriosis / Q000235:genetics* / Q000378:metabolism; D004717:Endometrium / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D005796:Genes / Q000187:drug effects; D006801:Humans; D008875:Middle Aged; D010750:Phosphoproteins / Q000235:genetics*; D000072317:Polychlorinated Dibenzodioxins / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D016601:RNA-Binding Proteins; D018336:Receptors, Aryl Hydrocarbon / Q000235:genetics*; D012016:Reference Values; D014157:Transcription Factors / Q000378:metabolism
chemical_list: C497396:ARNT protein, human; D004268:DNA-Binding Proteins; C489560:DOK1 protein, human; C074561:GAP-associated protein p62; D010750:Phosphoproteins; D000072317:Polychlorinated Dibenzodioxins; D012333:RNA, Messenger; D016601:RNA-Binding Proteins; D018336:Receptors, Aryl Hydrocarbon; D014157:Transcription Factors; D051784:Aryl Hydrocarbon Receptor Nuclear Translocator; D003577:Cytochrome P-450 Enzyme System; D001189:Aryl Hydrocarbon Hydroxylases; C585496:CYP1B1 protein, human; D065633:Cytochrome P-450 CYP1B1