CONICET | Buscador de Institutos y Recursos Humanos

The lactotroph cell population exhibits a remarkable rate of cell turnover in response to different physiological and experimental conditions. These changes in the number of PRL cells are characteristic of a dynamic population. The maintenance of homeostasis of lactotrophs population is regulated mainly for the tonic inhibition of dopamine and can be stimulated by actions of neuropeptides, steroid hormones and growth factors. Steroid hormones such as estradiol (E2) are involved in the balance of mitogenic activity of the lactotroph cells. The physiological functions of estrogen can be mediated by the classical citoplasmatic/nuclear estrogen receptors (ER), ER alpha and ER beta, which work as ligand-activated transcription factors. In addition, in previous works we have demonstrated that E2 through membrane estrogen receptor alpha (mER alpha) modulates the lactotroph cell population which exhibit noticeable changes in the pituitary gland. Several studies have described that the interaction between estradiol and growth factors (EGF or IGF-1) stimulate cell proliferation. We reported that the sustained administration of estradiol induced an increase in the production of basisc fibroblast growth factor (FGF-2) in experimental prolactinomas. In addition, it has been reported that E2 binding to its ER can promote proliferation modulating the activity of transcription factors and gene expression through two mechanisms: interacting with nuclear proteins or activating at transduction pathways initiated at the membrane plasma. The activation of these signaling pathways induced by E2 bound to membrane ER would be mediated for scaffolding molecules or by interaction with growth factors receptors. However, the convergence of the molecular mechanisms involved in rapid effects of E2 mediated by membrane ER and its genomic action in interaction with FGF-2 has not been described in the pituitary gland.