title: Expression of estrogen receptor-alpha, glucocorticoid receptor, beta-catenin and glycogen synthase kinase-3beta in the uterus of mice following long-term treatment with estrogen and glucocorticoid hormones.
abstract: BACKGROUND
  It has been shown that long-term glucocporticoid administration to chronically estradiol-treated mice decreases uterine weight, proliferation in all uterine tissues, the number of perpendicularly oriented mitoses in uterine epithelia and the incidence of atypical endometrial hyperplasia. However, mechanisms of chronic glucocorticoid action on estrogen-dependent processes in the uterus are unclear.
  
  
  RESULTS
  Results of present research showed that adding of glucocorticoid dexamethasone (in drinking water, 2mg/l) to estradiol-treated mice led to a decrease in the level of glucocorticoid receptor, to an increase in levels of estrogen receptor-alpha, beta-catenin and glycogen synthase kinase-3beta in uterine tissues of ovariectomized mice at 30, 60 and 90 days of the treatment. When vehicle was used instead estradiol, dexamethasone did not produce detectable changes in all parameters tested at all periods of observation.
  
  
  CONCLUSIONS
  Results allow to conclude that estrogen and glucocorticoid receptors, beta-catenin and glycogen synthase kinase-3beta are involved in estrogen-dependent changes in uterine morphology and hyperplasia formation.
authors.affiliation: Department of Histology, Medical School Chuvash State University, PO Box 86, Cheboksary 428034, Russia. drgunin@yahoo.com
authors.forename: Andrei G
authors.initials: AG
authors.lastname: Gunin
authors.forename: Vladimir U
authors.initials: VU
authors.lastname: Emelianov
authors.forename: Alexei S
authors.initials: AS
authors.lastname: Tolmachev
mesh_terms: D000818:Animals; D002467:Cell Nucleus / Q000737:chemistry; D003593:Cytoplasm / Q000737:chemistry; D003598:Cytoskeletal Proteins / Q000032:analysis*; D003907:Dexamethasone / Q000008:administration & dosage / Q000494:pharmacology; D004714:Endometrial Hyperplasia / Q000139:chemically induced; D004848:Epithelium / Q000737:chemistry; D004958:Estradiol / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D047628:Estrogen Receptor alpha; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D038362:Glycogen Synthase Kinase 3 / Q000032:analysis*; D000071679:Glycogen Synthase Kinase 3 beta; D007150:Immunohistochemistry; D051379:Mice; D010052:Ovariectomy; D011960:Receptors, Estrogen / Q000032:analysis*; D011965:Receptors, Glucocorticoid / Q000032:analysis*; D015534:Trans-Activators / Q000032:analysis*; D014599:Uterus / Q000737:chemistry / Q000187:drug effects / Q000648:ultrastructure; D051176:beta Catenin
chemical_list: C495267:CTNNB1 protein, mouse; D003598:Cytoskeletal Proteins; D047628:Estrogen Receptor alpha; D005938:Glucocorticoids; D011960:Receptors, Estrogen; D011965:Receptors, Glucocorticoid; D015534:Trans-Activators; D051176:beta Catenin; D004958:Estradiol; D003907:Dexamethasone; D000071679:Glycogen Synthase Kinase 3 beta; C000605507:Gsk3b protein, mouse; D038362:Glycogen Synthase Kinase 3