PKCepsilon/ERK1/2 PARTIPATION IN THE PROLIFERATIVE EFFECT OF ESTRADIOL IN INTERACTION WITH FGF-2 ON LACTOTROPHS

SOSA L.; GUTIÉRREZ S.; PETITI J.P.; PALMERI C.; DE PAUL A.L.; TORRES A.I.

Buenos Aires

Jornada; X Jornadas Anuales de la Sociedad Argentina de Biología; 2008

Sociedad Argentina de Biología

In previous studies we demonstrated that estradiol (E2) co-incubated with FGF-2 produced mitogenic effects in lactotroph cells. The objective of the present work was to evaluate the participation of PKCalpha, epsilon, delta and ERK1/2 on the lactotroph cell proliferation induced by E2/FGF-2 interaction. Primary pituitary cell cultures from female rats were treated with E2 (10nM) and FGF-2 (0.6 nM), alone or combined, for 4h. Lactotroph cell proliferation was determinate by ICQ (BrdU/PRL). Estrogen receptor (RE) alpha, PKCalpha, epsilon, delta and ERK1/2 total and phosphorylated (p) expressions were determinate by WB. FGF receptor (RFGF) was identified by immuno-electron-microscopy (ICQe). Statistical analysis: ANOVAFisher. The individual treatment with E2 or FGF-2 did not modify the lactotroph cell number compared to control, whereas that E2/FGF-2 combination significantly increased the mitogenic activity of these cells. RFGF was detected in pituitary cells. The REalpha and PKC alpha expression levels did not exhibit variation after treatments. PKC epsilon levels increased in similar way (p<0.01) in all experimental models compared to controls. E2/FGF-2 co-incubation induced the greater PKC epsilon expression and ERK1/2 activation. These results suggest that lactotroph cell proliferation induced by E2/FGF-2 interaction is mediated by PKCepsilon and ERK1/2.