title: TGF-beta 1 and IGF-1 expression in atrophic post-menopausal endometrium.
abstract: OBJECTIVE
  Endometrial cells may synthetize cytokines and growth factors which may modulate some of the molecular mechanisms of endometrial proliferation and differentiation.
  
  
  METHODS
  We investigated the role of transforming growth factor beta-1 (TGF-beta 1), insulin-like growth factor-1 (IGF-1) and relative receptors in five tissue samples from atrophic post-menopausal endometria. The control group was represented by proliferative and secretory endometria from 10 healthy, normally-menstratued women. TGF-beta 1 and IGF-1 m-RNA expression was evaluated by Northern hybridization analysis, while TGF-beta 1 and IGF-1 receptors distribution was studied by immunohistochemistry.
  
  
  RESULTS
  In atrophic endometria Northern hybridization analysis showed a significant decrease of IGF-1 expression, and an increase of TGF-beta 1 expression compared to proliferative and secretory endometria. By immunohistochemistry it was demonstrated that TGF-beta 1 and IGF-1 receptors were both localized in cell cytoplasm, mainly in the stromal compartment.
  
  
  CONCLUSIONS
  The results of our study would suggest a possible role of IGF-1 and TGF-beta 1 in maintaining the quiescent differentiative state of atrophic post-menopausal endometrium. The persistence of IGF-1 and TGF-beta 1 receptors in epithelial compartment could play a key role in proliferative response of atrophic endometrium to exogenous hormone replacement therapy (HRT) or endogenous intervening high estrogens levels.
authors.affiliation: Department of Obstetrics and Gynaecology, School of Medicine, University of Bari, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Loverro
authors.forename: E
authors.initials: E
authors.lastname: Perlino
authors.forename: E
authors.initials: E
authors.lastname: Maiorano
authors.forename: G
authors.initials: G
authors.lastname: Cormio
authors.forename: R
authors.initials: R
authors.lastname: Ricco
authors.forename: E
authors.initials: E
authors.lastname: Marra
authors.forename: L
authors.initials: L
authors.lastname: Nappi
authors.forename: T
authors.initials: T
authors.lastname: Giannini
authors.forename: L
authors.initials: L
authors.lastname: Selvaggi
mesh_terms: D000328:Adult; D000818:Animals; D001284:Atrophy; D015152:Blotting, Northern; D016022:Case-Control Studies; D004717:Endometrium / Q000166:cytology* / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D051379:Mice; D008875:Middle Aged; D017698:Postmenopause; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D017526:Receptor, IGF Type 1 / Q000235:genetics / Q000378:metabolism*; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism*
chemical_list: D012333:RNA, Messenger; D018125:Receptors, Transforming Growth Factor beta; D017526:Receptor, IGF Type 1