Association between macrophage migration inhibitory factor in the endometrium and estrogen in endometriosis

被引:17
作者
Zhang, Xiao [1 ]
Mu, Lin [2 ]
机构
[1] Zhejiang Univ, Sch Med, Sir Run Run Shaw Hosp, Dept Gynecol, Hangzhou 310000, Zhejiang, Peoples R China
[2] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Gynecol, Hangzhou 310000, Zhejiang, Peoples R China
基金
中国国家自然科学基金;
关键词
endometriosis; eutopic endometrium; macrophage migration inhibitory factor; estrogen; 17; beta-estradiol; TUMOR-ASSOCIATED ANGIOGENESIS; FACTOR MIF; MENSTRUAL-CYCLE; DISEASE STAGE; EXPRESSION; INFERTILITY; GROWTH; WOMEN; HYPERSENSITIVITY; TISSUE;
D O I
10.3892/etm.2015.2516
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Recent studies have shown that macrophage migration inhibitory factor (MIF) has a possible role in endometriosis-related pain and infertility, yet it has not been explored whether the mRNA level of MIF is altered in endometrial tissues from patients with endometriosis. The aim of the present study was to compare the expression of MIF in endometrial tissues from women with and without endometriosis, and to analyze the association between endometrial MIF expression and 17 beta-estradiol (E-2). The protein and mRNA expression of MIF in the human endometrial tissue was assessed by western blotting and reverse transcription-polymerase chain reaction analysis, respectively. The MIF expression of women with endometriosis was found to be significantly higher than that of the controls. A positive correlation was noted between the serum E-2 level and MIF expression. In endometrial cells from women with endometriosis, the level of E-2-induced MIF upregulation was significantly higher than that in cells from women without endometriosis. In conclusion, this study demonstrated a significant increase in MIF expression in the endometrial tissues of women with endometriosis and an association between MIF expression and E-2 level. MIF expression in endometrial cells from patients with endometriosis showed an increased sensitivity to stimulation by E-2.
引用
收藏
页码:787 / 791
页数:5
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