国际妇产科学杂志 ›› 2015, Vol. 42 ›› Issue (5): 500-503.

• 论著 • 上一篇    下一篇

ER与TrkB在子宫内膜异位症患者不同子宫内膜组织中的表达

雍敏婕,李文倩,王芳,金伟,刘波,于晓辉   

  1. 116033 大连市妇幼保健院暨大连医科大学附属妇产医院妇科(雍敏婕,李文倩,王芳,于晓辉);大连市友谊医院药剂科(金伟);大连理工大学生物医学工程系(刘波)
  • 收稿日期:1900-01-01 修回日期:1900-01-01 出版日期:2015-10-15 发布日期:2015-10-15
  • 通讯作者: 于晓辉

Expression of ER and TrkB in Endometriosis

YONG Min-jie,LI Wen-qian,WANG Fang,JIN Wei,LIU Bo,YU Xiao-hui   

  1. Department of Gynecology,Dalian Obstetrics and Gynecology Hospital Affiliated to Dalian Medical University,Dalian 116033,Liaoning Province,China(YONG Min-jie,LI Wen-qian,WANG Fang,YU Xiao-hui);Department of Pharmacy,Dalian Friendship Hospital Affiliated to Dalian Medical University,Dalian 116001,Liaoning Province,China(JIN Wei);Department of Biomedical Engineering,Dalian University of Technology,Dalian 116024,Liaoning Province,China(LIU Bo)
  • Received:1900-01-01 Revised:1900-01-01 Published:2015-10-15 Online:2015-10-15
  • Contact: YU Xiao-hui

摘要: 目的:检测雌激素受体(ER)和酪氨酸激酶受体B(TrkB)在子宫内膜异位症(EMs)患者在位和异位内膜组织中的表达,评价ER和TrkB在EMs发病中的作用。方法:选择18例卵巢EMs病例,其中在位内膜增殖期9例、分泌期9例。采用实时聚合酶链反应(real time PCR)、蛋白质印迹法(Western blotting)和免疫组织化学法检测ERα、ERβ、TrkB和脑源性神经营养因子(BDNF)mRNA和蛋白质的表达。结果:EMs患者在位内膜ERα mRNA和蛋白表达高于异位内膜组织,而ERβ、TrkB mRNA和蛋白的表达均低于异位内膜组织,差异有统计学意义(均P<0.05)。异位内膜组织中ERβ/ERα mRNA的比值高于在位内膜组。在EMs在位内膜中,ERα、ERβ、TrkB蛋白的表达在增殖期均高于分泌期(均P<0.05)。ERα主要表达于在位内膜细胞核内;ERβ主要表达于异位内膜细胞质中;ERα与ERβ在EMs在位内膜的增殖期着色比分泌期更加明显。EMs的在位内膜和异位内膜组织中TrkB与BDNF都有表达,且主要集中于细胞质。EMs在位内膜中TrkB蛋白质在增殖期表达更明显。结论:ERβ和TrkB可能在EMs的发病机制中发挥作用。

关键词: 受体, 雌激素, 受体, trkB, 子宫内膜异位症, 子宫内膜

Abstract: Objective:To detect the expression of estrogen receptor (ER) and TrkB in eutopic endometrium and ectopic endometrium in patients with endometriosis, and explore the potential effect of ER and TrkB in the pathogenesis of EMs. Methods:The expressions of ERα, ERβ, TrkB and BDNF in 18 cases with EMs (include 9 proliferating phase cases and 9 secretory phase of eutopic endometrium) were examined using real-time PCR, Western blotting and immunohistochemistry. Results:At mRNA and protein levels, the expression of ERα in eutopic endometrium was higher than ectopic endometrium with endometriosis, while the expression of ERβ and TrkB in eutopic endometrium were lower than ectopic endometrium with endometriosis, all of that difference have statistically significant (P<0.05). Higher ratio of ERβ/ERα mRNA was found in ectopic endometriosis than eutopic endometrium. In eutopic endometrium, ERα, ERβ and TrkB proteins were mainly expressed in proliferative phase than that in secretory phase (P<0.05). ERα expression was mainly found in cell nucleus of eutopic endometrium, while ERβ was mainly found in cytoplasm of ectopic endometrium. The expression of ERα and ERβ were more obvious in EMs eutopic endometrium proliferative phase than that in secretory phase. TrkB and BDNF were expressed in both eutopic and ectopic endometrium with EMs, and were mainly expressed in cytoplasm. TrkB was more obvious in proliferative phase eutopic endometrium of EMs. Conclusions:ERβ and TrkB may mediate the pathogenesy of EMs.

Key words: Receptors, estrogen, Receptor, trkB, Endometriosis, Endometrium