Regulation of myeloid ecotropic viral integration site 1 and its expression in normal and abnormal endometrium
Regulation of myeloid ecotropic viral integration site 1 and its expression in normal and abnormal endometrium
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髓系亲嗜性病毒整合位点1的调节及其在正常和异常子宫内膜中的表达。
DOI：
10.1016/j.fertnstert.2014.05.036
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发表时间：
2014-09-01
影响因子：
6.7
通讯作者：
Qian, Kun
中科院分区：
文献类型：
--
作者：
Hu, Linli;Li, Haixia;Qian, Kun
目的：确定子宫内膜中骨髓共嗜性病毒整合位点 1 (MEIS1) 的表达谱和性类固醇调节模式。设计：人类和动物组织中的分子研究。地点：大学医院生殖医学中心。患者和动物：月经周期正常的男性不孕症女性不孕症和女性不孕症合并子宫内膜异位症。性成熟雌性小鼠（昆明白系）。干预措施：原代培养的子宫内膜基质细胞、石川细胞和卵巢切除的小鼠用性类固醇治疗。主要结果指标：分析月经周期期间人子宫内膜、妊娠围着床期小鼠子宫和子宫内膜异位症患者在位子宫内膜中 MEIS1 的表达。免疫组织化学染色和蛋白质印迹。此外，通过免疫组织化学染色和蛋白质印迹在体外和体内检查了性类固醇反应中的 MEIS1 表达。结果：着床期间的子宫内膜以及人子宫内膜和小鼠子宫的蜕膜化基质细胞中 MEIS1 表达显着增加。类固醇激素增加了原代培养的子宫内膜基质细胞、石川细胞和卵巢切除小鼠子宫内膜中 MEIS1 的表达。雌激素和黄体酮的作用在卵巢切除小鼠中更为明显，并且是相加的。在分泌中期，MEIS1在在位子宫内膜中的表达显着低于正常子宫内膜。结论：MEIS1可能是性类固醇和子宫容受性基因之间的关键调节因子。子宫内膜 MEIS1 表达减少可能导致子宫内膜异位症植入失败。 (C) 2014 年，美国生殖医学会。
Objective: To identify the expression profile and sex steroid regulation pattern of myeloid ecotropic viral integration site 1 (MEIS1) in endometrium.Design: Molecular studies in human and animal tissue.Setting: Reproductive medicine center of a university hospital.Patient(s) and Animal(s): Women with normal menstrual cycles for male infertility and female infertility with endometriosis. Sexually mature female mice (Kunming White strain).Intervention(s): Primary cultured endometrial stromal cells, Ishikawa cells, and oophorectomized mice were treated with sex steroid.Main Outcome Measure(s): MEIS1 expression in the human endometrium during the menstrual cycle, mouse uterus during the peri-implantation period of pregnancy, and eutopic endometrium from patients with endometriosis was analyzed by immunohistochemistry staining and western blot. In addition, MEIS1 expression in response to sex steroid was examined both in vitro and in vivo by immunohistochemistry staining and western blot.Result(s): MEIS1 expression was markedly increased in endometrium during the implantation period, and in decidualizing stromal cells in human endometrium and murine uterus. Steroid hormones increased MEIS1 expression in primary cultured endometrial stromal cells, Ishikawa cells, and endometrium of oophorectomized mice. The effects of estrogen and progesterone were more marked in oophorectomized mice and were additive. MEIS1 expression was significantly lower in eutopic endometrium compared with normal endometrium in the midsecretory stage.Conclusion(s): MEIS1 is likely a key mediator between sex steroid and genes for uterine receptivity. Diminished endometrium MEIS1 expression may contribute to implantation failure in endometriosis. (C) 2014 by American Society for Reproductive Medicine.