Study On Distribution Of Estrogen Receptor Isoforms And Relationship With Dysmenorrhea Factors In Endometriosis

Objective: To investigate the distribution of estrogen receptor isoforms and dysmenorrhea factors COX-2 and OTR in eutopic and ectopic endometrium in endometriosis and adenomyosis, also the relationship between estrogen receptor isoforms and dysmenorrhea factors was discussed.Methods: Samples of endometrium and ovarian endometriosis cysts were collected and divided into 5 groups: eutopic endometrium of endometriosis(30 cases), ovarian endometriosis cysts(30 cases), eutopic endometrium of adenomyosis(30 cases), adenomyotic lesion(30 cases), normal endometrium(20 cases). Employed immunohistochemical method to investigate the expression of ER α ,ER β ,COX-2 and OTR in different tissue and cells and during menstrual cycle.Results: 1,Expression of ER α in eutopic endometrium was significantly higher than ovary endometrisis cyst in endometriosi (73.3% to 43.3% respectively, P<0.05), but expression of ER β was higher in ovary endometrisis cyst than eutopic ( 90% to 68% respectively, P < 0.05) and normal endometrium(35%). Expression of ER α was same as ER β in adenomyosis. In ademyotic lesion and eutopic endometrium, there were higher level comparing with normal endometrium, P<0.05. For endometriosis and adenomyosis, ER α and ER β level changed periodically in endometrium. During the proliferation, both of ER α and ER β were higher than in secreted duration, whereas ER α and ER β level were less variable in proliferate and secreted duration for the ectopic lesion in endometriosis and adenomyosis . 2, Both ovary endometriosis cyst and adenomyotic lesion showed predominantly higher levels of expression of COX-2 than that in eutopic and normal endometrium in endometriosis and adenomyosis (P <0.05). The expressive rate of COX-2 was higher in eutopic endometriumduring the secretion than that in the proliferation, whereas there was a less periodical variation of COX-2 in the ectopic lesion in endometriosis and adenomyosis. The expression of COX-2 in ectopic lesion with endometriosis and ademyosis was higher in the group with dysmenorrhea than those without or mild dysmenorrhea (P <0.05). 3,Both ovary endometriosis cyst and adenomyotic lesion showed predominantly higher levels of OTR than that in eutopic and normal endometrium in endometriosis and adenomyosis(P < 0.05). The expressive rate of OTR was higher in eutopic endometrium during the proliferation than that in the secretion, where as there was a less periodical variation of OTR expression in the ectopic lesion in endometriosis and adenomyosis. The expression of OTR in ectopic lesion with endometriosis and adenomyosis was higher in the group with dysmenorrhea than those without or mild dysmenorrhea. 4,Expression of COX-2 and OTR were relevant to ERβ in ovary endometriosis cyst, whereas were relevant to ERα and ERβ in adenomyotic lesion.Conclusion: 1,For endomertiosis, ERα was high in eutopic endometrium and in ovary endometrisis cyst ERβ was high when ERα level was limited, thus we speculated the predominant expression of ERβ may be essential for the development and growth of ovary endometriosis cyst; where as ERα and ERβ may play key role in the development and growth of adenomyosis due to ER α and ERβ higher in adenomyotic lesion than in eutopic and normal endometrium in adenomyosis. 2,The abundant expression of COX-2 in ectopic and eutopic endometrium hint COX-2 may be involved in the development and growth of endometriosis and adenomyosis , and is tightly relevant to the complaint of dysmenorrhea. 3, The strong expression of OTR in ectopic and eutopic endometrium hint OTR may be involved in the development and growth of endometriosis and adenomyosis. The association of OTR with dysmenorrhea suggests an involvement of the OTR system in the development of endometriosis-associated symptoms such as pelvic pain and/or dysmenorrhea. 4, From the correlation between COX-2 and OTR relative with ER α and ER β, wespeculated that estrogen may upregulate the expression of COX-2 and OTR via ERβ in ovary endometriosis cyst but via ER α and ER β in adenomyosis.