Estradiol Stimulates Vascular Endothelial Growth Factor and Interleukin-6 in Human Lactotroph and Lactosomatotroph Pituitary Adenomas

Estrogens are considered to be critically involved in lactotroph and lactosomatotroph pituitary tumor development. In addition to direct effects, estradiol-induced tumor formation may involve alterations in growth factor and cytokine production. We have studied whether estradiol stimulates the produ...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autor principal: Carbia Nagashima, Alberto Nicolás
Publicado: 2004
Materias:
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09477349_v112_n1_p18_Onofri
http://hdl.handle.net/20.500.12110/paper_09477349_v112_n1_p18_Onofri
Aporte de:
Descripción
Sumario:Estrogens are considered to be critically involved in lactotroph and lactosomatotroph pituitary tumor development. In addition to direct effects, estradiol-induced tumor formation may involve alterations in growth factor and cytokine production. We have studied whether estradiol stimulates the production of the angiogenic vascular endothelial growth factor and the potential tumor progression factor interleukin-6 in 5 lactotroph (LA) and 5 lactosomatotroph (LSA) human pituitary adenoma cell cultures. All tumors secreted heterogenous basal amounts of VEGF (18.0 ± 1.4 to 425 ± 26 pg/ml per 24h) and IL-6 (18.1 ± 1.5 to 604 ± 17 pg/ml per 24h). Estradiol (100nM) significantly enhanced VEGF release in all LA and LSA cell cultures (47 to 168% above basal). IL-6 secretion was stimulated in 3 out of 5 LA and in all LSA cell cultures (31 to 287% above basal). In cell cultures obtained from tumors from which sufficient cells could be isolated, a dose-dependent effect of estradiol (1 to 100 nM) on VEGF and IL-6 production was observed. Stimulation of IL-6 and/or VEGF secretion by estradiol in the majority of human lactotroph and lactosomatotroph adenoma cell cultures studied, suggests that estrogens may contribute to adenoma expansion through the stimulation of these auto-/paracrine-acting adenoma progression factors.