| Research Abstract |
Estrogen dependence and immune modulations are established features of endometriosis, and environmental contaminants have been suggested to play a role in the pathobiology of endometriosis. Previous work in nonhuman primates has shown that exposure to the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is associated with an increased prevalence and severity of endometriosis. The effects of dioxins are mediated via the arylhydrocarbon receptor(AHR), aryl hydrocarbon receptor nuclear receptor nuclear translocator(ARNT), and aryl hydrocarbon receptor repressor(AHRR).
We identified and characterized the human homolog of mouse AHRR, taking advantage of the publicly available draft version of the human genome sequence. After detecting the AHRR polymorphism, the genetic polymorphism of AHR, ARNT were also investigated. We explored the association of the AHR, ARNT, and AHRR polymorphism with endometriosis in a case-control study. Although no significant correlation was found between endometriosis and polymorphism of AHR, ARNT, or AHRR genes, pathological phenotypes of endometriosis may be associated with the dioxin related genes other than AHR, ARNT, and AHRR.
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