Objectives: Endometrial cells may synthetize cytokines and growth factors which may modulate some of the molecular mechanisms of endometrial proliferation and differentiation.
Patients and 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.