title: Steroid receptors ERalpha, ERbeta, PR-A and PR-B are differentially expressed in normal and atrophic human endometrium.
abstract: The endometrium expresses estrogen (ER) and progesterone receptor (PR), which are related to autocrine and paracrine processes that respond to estrogen and progesterone. Therefore, the aim of this study was to evaluate the distribution pattern of ERalpha, ERbeta, PR-A and PR-B with monoclonal antibodies in normal human endometrial tissue.
  
  
  
  Human endometrial tissue was obtained from 84 premenopausal and 11 postmenopausal patients and immunohistochemically analysed with monoclonal antibodies against ERalpha, ERbeta, PR-A and PR-B.
  
  
  
  ERalpha, PR-A and PR-B declined significantly (p<0.001, p<0.05, p<0.05 respectively) in glandular epithelium from proliferative to late secretory phase. The ERbeta immunohistochemical reaction showed a similar significant declining pattern (p<0.05), although the staining intensity was lower than that of ERalpha. While ERalpha, ERbeta and PR-B decrease significantly in atrophic endometrial tissue compared to proliferative endometrium, a significant up-regulation of PR-A was observed compared to late secretory phase (p<0.05).
  
  
  
  ERalpha, ERbeta, PR-A and PR-B were expressed in normal human endometrium with a cyclical variation during the menstrual cycle. In normal postmenopausal endometrial tissue, a down-regulation of ERalpha, ERbeta and PR-B occurs with a subsequent higher expression of PR-A. These results show the presence of steroid receptors in human epithelium, indicating that these cells respond to estrogen and progesterone, thus playing a significant role in endometrial physiology.
authors.affiliation: First Department of Obstetrics and Gynaecology, Ludwig-Maximilians, University Munich, Germany.
authors.forename: I
authors.initials: I
authors.lastname: Mylonas
authors.forename: U
authors.initials: U
authors.lastname: Jeschke
authors.forename: N
authors.initials: N
authors.lastname: Shabani
authors.forename: C
authors.initials: C
authors.lastname: Kuhn
authors.forename: S
authors.initials: S
authors.lastname: Kunze
authors.forename: D
authors.initials: D
authors.lastname: Dian
authors.forename: C
authors.initials: C
authors.lastname: Friedl
authors.forename: M S
authors.initials: MS
authors.lastname: Kupka
authors.forename: K
authors.initials: K
authors.lastname: Friese
mesh_terms: D001284:Atrophy / Q000473:pathology; D015415:Biomarkers / Q000378:metabolism; D004717:Endometrium / Q000378:metabolism* / Q000473:pathology; D047628:Estrogen Receptor alpha / Q000378:metabolism*; D047629:Estrogen Receptor beta / Q000378:metabolism*; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D008597:Menstrual Cycle / Q000502:physiology; D017697:Premenopause; D011980:Receptors, Progesterone / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D011980:Receptors, Progesterone; C101118:progesterone receptor A; C097314:progesterone receptor B