Aims: Endometriosis (EM) is a hormone-dependent chronic inflammatory disease, usually accompanied by a high level of localized estrogen and abnormal levels of cytokines, which are regulated by GATA-3 in lymphocytes. This study aimed to investigate the role of estrogen on GATA-3 expression and the relationship between GATA-3 and cytokine response. Methods: Endometrial tissues collected from 20 patients who underwent laparoscopic or open surgery were used. Immunohistochemistry, quantitative polymerase chain reaction, Western blot analysis, cell transfection, estrogen treatments and enzyme-linked immunosorbent assays were performed to evaluate the effects of estrogen on GATA-3 expression and the relationship between estrogen-induced GATA-3 and the Th2 immune status of EM. Results: Estrogen regulated the expression of GATA-3 in a dose and time-dependent manner. GATA-3 was relocated from the cytoplasm to the nucleus. Estrogen and GATA-3 regulated Th2 cytokine expression in eutopic endometrial cells, including interleukin (IL)-6, IL-8 and IL-10. Moreover, interferon-γ and IL-2 were highly expressed in the GATA-3 knockdown groups. Conclusion: In summary, GATA-3 was induced by estrogen and may promote the occurrence and development of EM by regulating the secretion of cytokines in the eutopic endometrial cells of EM patients.
The objective was to investigate the expression of the WNT4 gene in ectopic endometrium and eutopic endometrium (EU) during endometriosis and the relationship of WNT4 expression with the menstrual cycle. Ectopic endometrium and EU tissues were collected from 30 women with pathologically confirmed endometriosis and 30 women without endometriosis. The WNT4 protein and messenger RNA (mRNA) expression levels were measured by fluorescence-based quantitative real-time polymerase chain reaction, immunohistochemistry, and Western blot methods. The expression of WNT4 was not significantly correlated with the menstrual cycle, and there were no significant differences when WNT4 expression in proliferative endometrium was compared with that in secretory endometrium within each group. There were no significant differences between the protein and mRNA expression of WNT4 in ectopic endometrium and in EU from participants with endometriosis. The WNT4 expression level in EU was significantly reduced compared with that in normal endometrium of the control group, even when analyzed by the menstrual cycle phase. WNT4 was also downregulated in ectopic lesions. This study provides further evidence supporting the theory of "EU determinism" in the pathogenesis of endometriosis.
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