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Role of estrogen, estrogen receptors, and aromatase in the pathogenesis of uterine adenomyosis / 南方医科大学学报
Article em Zh | WPRIM | ID: wpr-273756
Biblioteca responsável: WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To study the role of estrogen (E2), estrogen receptor (ER) and aromatase (P450arom) in the pathogenesis of uterine adenomyosis.</p><p><b>METHODS</b>Paraffin-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.</p><p><b>RESULTS</b>The 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).</p><p><b>CONCLUSION</b>The 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.</p>
Texto completo: 1 Índice: WPRIM Tipo de estudo: Etiology_studies Idioma: Zh Revista: Journal of Southern Medical University Ano de publicação: 2017 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Tipo de estudo: Etiology_studies Idioma: Zh Revista: Journal of Southern Medical University Ano de publicação: 2017 Tipo de documento: Article