info:eu-repo/semantics/article
Cooperative effect of E2 and FGF2 on lactotroph proliferation triggered by signaling initiated at the plasma membrane
Fecha
2013-04Registro en:
Sosa, Liliana del Valle; Gutiérrez, Silvina; Petiti, Juan Pablo; Vaca, Alicia Maldré del Valle; de Paul, Ana Lucia; et al.; Cooperative effect of E2 and FGF2 on lactotroph proliferation triggered by signaling initiated at the plasma membrane; American Physiological Society; American Journal Of Physiology-endocrinology And Metabolism; 305; 1; 4-2013; 45-49
0193-1849
1522-1555
Autor
Sosa, Liliana del Valle
Gutiérrez, Silvina
Petiti, Juan Pablo
Vaca, Alicia Maldré del Valle
de Paul, Ana Lucia
Torres, Alicia Ines
Resumen
In the present work, we investigated the effect of 17β-estradiol (E2) and basic fibroblast growth factor 2 (FGF2) on the lactotroph cell-proliferative response and the related membrane-initiated signaling pathway. Anterior pituitary mixed-cell cultures of random, cycling 3-mo-old female rats were treated with 10 nM E2, E2 membrane-impermeable conjugated BSA (E2-BSA), PPT (ERα agonist), and DPN (ERβ agonist) alone or combined with FGF2 (10 ng/ml) for 30 min or 4 h. Although our results showed that the uptake of BrdU into the nucleus of lactotrophs was not modified by E2 or FGF2 alone, a significant increase in the lactotroph uptake of BrdU was observed after E2/FGF2 coincubation, with this effect being mimicked by PPT/FGF2. These proliferative effects were blocked by ICI 182,780 or PD-98059. The involvement of membrane ER in the proliferative response of prolactin cells induced by the steroid and FGF2 coincubation was confirmed using E2-BSA, and the association between ERα and FGF receptor was observed after E2/FGF2 treatment by immunoprecipitation. A significant increase in the ERK1/2 expression was noted after E2, E2-BSA, PPT, and FGF2 alone, which was more noticeable after E2-BSA/FGF2, E2/FGF2, or PPT/FGF2 treatments. This study provides evidence that E2 and FGF2 exert a cooperative effect on the lactotroph proliferation principally by signaling initiated at the plasma membrane triggering a genomic effect mediated by MEK/ERK1/2, a common signaling pathway, that finally regulates the lactotroph population, thus contributing to pituitary plasticity.