Gonadotropm-releasing hormone and gonadotropin-releasing hormone receptor are expressed at tubal ectopic pregnancy implantation sitesl;
Gonadotropm-releasing hormone and gonadotropin-releasing hormone receptor are expressed at tubal ectopic pregnancy implantation sitesl;
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DOI：
10.1016/j.fertnstert.2016.02.003
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发表时间：
2016-06-01
影响因子：
6.7
通讯作者：
Bedaiwy, Mohamed A.
中科院分区：
文献类型：
--
作者：
Peng, Bo;Klausen, Christian;Bedaiwy, Mohamed A.
目的：研究促性腺激素释放激素(GnRH)及其受体(GnRHR)在输卵管妊娠部位的表达，探讨GnRH信号在调节永生化人滋养层细胞活性中的作用。设计：免疫组织化学和实验研究。地点：学术研究实验室。患者(S)：来自输卵管妊娠患者的输卵管植入部位(n=25)。采用免疫组织化学和组织化学方法检测GnRH和GnRHR的表达。干预(S)：无。主要观察指标(S)：GnRH和GnRHR的表达。用促性腺激素释放激素和(或)促性腺激素释放激素拮抗剂(安替)孵育滋养细胞BeWo绒毛膜癌和永生化绒毛外滋养细胞(HTR-8/SVneo)。结果：所有输卵管妊娠患者的细胞滋养层、合体滋养层和绒毛外滋养层细胞均表达GnRH和GnRHR免疫反应。合体滋养层细胞的GnRH免疫反应性高于细胞滋养层，GnRHR免疫反应性低于细胞滋养层。GnRH和GnRHR免疫反应阳性表达于邻近输卵管上皮细胞。而GnRH和ANTID均不影响HTR-8/SVneo细胞的活力，GnRH处理后48h和72h，BeWo细胞的总体细胞活力显著增加，这种作用可被安替比妥钠阻断。结论：GnRH和GnRHR在输卵管妊娠部位的滋养层细胞群和输卵管上皮细胞中均有表达。GnRH可提高BeWo细胞的活力，这种作用是由GnRHR介导的。需要进一步的工作来研究GnRH信号在异位妊娠中的潜在作用。(Fertil Steril(R)2016；105：1620-7。(C)美国生殖医学会2016年。)
Objective: To investigate whether gonadotropin-releasing hormone (GnRH) and GnRH receptor (GnRHR) are expressed at tubal ectopic pregnancy sites, and to study the potential role of GnRH signaling in regulating immortalized human trophoblast cell viability.Design: Immunohistochemical and experimental studies.Setting: Academic research laboratory.Patient(s): Fallopian tube implantation sites (n = 25) were collected from women with ectopic pregnancy. First-trimester human placenta biopsies (n = 5) were obtained from elective terminations of pregnancy.Intervention(s): None.Main Outcome Measure(s): GnRH and GnRHR expression was examined by means of immunohistochemistry and histoscoring. Trophoblastic BeWo choriocarcinoma and immortalized extravillous trophoblast (HTR-8/SVneo) cell viability was examined by means of cell counting after incubation with GnRH and/or GnRH antagonist (Antide).Result(s): GnRH and GnRHR immunoreactivity was detected in cytotrophoblast, syncytiotrophoblast, and extravillous trophoblast in all women with tubal pregnancy. GnRH immunoreactivity was higher and GnRHR immunoreactivity lower in syncytiotrophoblast compared with cytotrophoblast. GnRH and GnRHR immunoreactivity was detected in adjacent fallopian tube epithelium. Whereas neither GnRH nor Antide altered HTR-8/SVneo cell viability, treatment with GnRH significantly increased the overall cell viability of BeWo cells at 48 and 72 hours, and these effects were abolished by pretreatment with Antide.Conclusion(s): GnRH and GnRHR are expressed in trophoblast cell populations and fallopian tube epithelium at tubal ectopic pregnancy sites. GnRH increases BeWo cell viability, an effect mediated by the GnRHR. Further work is required to investigate the potential role of GnRH signaling in ectopic pregnancy. (Fertil Steril(R) 2016;105:1620-7. (C) 2016 by American Society for Reproductive Medicine.)