title: [Temporal and spatial expression of estrogen activity-related molecules in eutopic endometrium of adenomyosis].
abstract: OBJECTIVE
  The aim of this study was to demonstrate the temporal and spatial expression of estrogen receptor (ER), 17beta-hydroxysteroid dehydrogenase (17beta-HSD) in uterine endometria and the endometrial-myometrial interface (EMI) of adenomyosis and the effects of estrogen activity-related molecules on the occurrence of adenomyosis.
  
  
  METHODS
  Thirty-three cases of normal endometria (and myometrial) and eighteen cases of endometria (and myometrial) with adenomyosis were collected. Immunohistochemical assay was performed to locate the ERalpha, ERbeta, 17beta-HSDI and 17beta-HSDII in endometria and EMI.
  
  
  RESULTS
  The ERalpha positive cell number in glandular epithelial cells at the early proliferative phase increased evidently in adenomyosis (90%), while it was 60% in normal endometria. We found ERalpha signal in cytoplasm in glandular epithelial cells of adenomyosis endometria as well as in nucleus. Compared with normal endometrium (early proliferative phase: +; late proliferative phase: ++; late secretory phase: +), eutopic endometrium with adenomyosis exhibited a higher level of 17beta-HSDI (early proliferative phase: ++; late proliferative phase: +++; late secretory phase: ++). The intensity of 17beta-HSDIIin glandular epithelial cells of eutopic endometrium with adenomyosis (early proliferative phase: +++; secretory phase: ++++) was also higher than that of normal endometrium (early proliferative phase: - approximately ++; secretory phase: +++). Higher intensities of ERalpha, ERbeta and 17beta-HSDIand lower intensities of 17beta-HSDII were observed in EMI than in the eutopic endometrium of adenomyosis.
  
  
  CONCLUSIONS
  The elevation of ERalpha positive cell number, 17beta-HSDI level as well as the insufficient compensation of 17beta-HSDII in eutopic endometrium with adenomyosis and the change in expression pattern of ERalpha, ERbeta, 17beta-HSDI and 17beta-HSDII in EMI lead to the local enhancement of estrogen effect, which would promote cell proliferation.
authors.affiliation: State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, China & Bioactive Materials Key Laboratory of Ministry of Education, Life Science College, Nankai University, Tianjing 200000, China.
authors.forename: Zhi-rong
authors.initials: ZR
authors.lastname: Guo
authors.forename: Ju
authors.initials: J
authors.lastname: Zhang
authors.forename: Jing-he
authors.initials: JH
authors.lastname: Lang
authors.forename: Jin-hua
authors.initials: JH
authors.lastname: Leng
authors.forename: Yun-shang
authors.initials: YS
authors.lastname: Piao
authors.forename: Yan-ling
authors.initials: YL
authors.lastname: Wang
mesh_terms: D015067:17-Hydroxysteroid Dehydrogenases / Q000032:analysis*; D000328:Adult; D002828:Choristoma / Q000378:metabolism* / Q000473:pathology; D004715:Endometriosis / Q000378:metabolism* / Q000473:pathology; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008597:Menstrual Cycle / Q000378:metabolism; D008875:Middle Aged; D011960:Receptors, Estrogen / Q000032:analysis*
chemical_list: D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D011960:Receptors, Estrogen; D015067:17-Hydroxysteroid Dehydrogenases; C044256:3 (or 17)-beta-hydroxysteroid dehydrogenase