OBJECTIVETo study the role of estrogen (E2), estrogen receptor (ER) and aromatase (P450arom) in the pathogenesis of uterine adenomyosis.

METHODSParaffin-embedded specimens of the uterine tissue from patients with uterine adenomyosis and patients with cervical lesions (CIN; control) were examined for expressions of E2, ER and P450arom by immunohistochemistry and ELISA. The cells isolated from the lesions of patients with adenomyosis were cultured in vitro, and the changes in cell growth in response to treatments with E2, ER inhibitor, ER inhibitor + E2, estrogen deprivation, and estrogen deprivation+ ICI182780 were assessed using CCK-8 method.

RESULTSThe expression levels of E2, ER, and P450arom were significantly higher in adenomyosis ectopic lesions and eutopic endometrium than in the myometrium and endometrium in the control group (P<0.05); no significant difference in E2 and P450arom expressions was found between adenomyosis ectopic lesions and eutopic endometrium (P>0.05), while the expression levels of ER in ectopic lesions was significantly higher than that in eutopic endometrium. The cell inhibition rates were similar between ER inhibitor group and ER inhibitor + Estrogen activation group (P>0.05), and was significantly higher in estrogen deprivation+ ER inhibitor group than in estrogen deprivation group (P<0.05).

CONCLUSIONThe high expression levels of E2, ER, and P450arom in adenomyosis ectopic lesions and eutopic endometrium promote uterine adenomyosis cell proliferation, in which process E2 combines with ER to execute its biological effect; ER also promotes the occurrence and development of uterine adenomyosis through other pathways.