Basic Fibroblast Growth Factor in hyperplastic pituitaries of dopamine receptor D2 knockout female mice

CAROLINA CRISTINA; PÉREZ MILLÁN M. INÉS; GRACIELA DÍAZ-TORGA; ADRIAN GONGORA; ALBERTO BALDI; GABRIELA SYCZ; DAMASIA BECÚ-VILLALOBOS

Miami

Congreso; 89th annual meeting Endocrine 2007; 2007

Endocrine Society

Dopamine D2 Receptor knockout (KO) female mice develop chronic hyperprolactinemia and pituitary hyperplasia. Recently, we have shown that they have an overexpression of vascular endothelial growth factor (VEGF) in folliculoestellate cells, suggesting a paracrine action of VEGF on pituitary endothelial cells (Endocrinology 146:2952:2005). Numerous growth factors modulate angiogenesis in different conditions. Among them, the type-2 Fibroblast Growth Factor (FGF2) exerts its mitogenic action on a wide variety of cells. We studied the expression of FGF2 and its receptor, FGFR1, in pituitaries from KO and wildtype (WT) female mice. We also evaluated FGF2 subcellular localization in relation to the development of pituitary hyperplasia, the effect of FGF2 on prolactin secretion, cell proliferation and phosphorylation of extracellular signal-regulated kinases (ERK) comparatively in pituitaries from WT and KO 8 month-old female mice. 1 and 10 ng/ml FGF2-induced prolactin release showed a similar pattern in both genotypes, even though basal release was higher in KOs. 10 ng/ml FGF2 stimulated pituitary cellular proliferation (MTS assay and 3[H]-Thymidine incorporation), and there were no differences between genotypes (P Interaction= 0.82, FGF: P= 0.0061 and 0.0042, respectively). The concentration of FGF2 (measured by ELISA) was lower in KO pituitaries (P