ERK1/2 AND p38 ACTIVATION IN NON-APOPTOTIC CELL DEATH INDUCED BY BROMOCRIPTINE

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

Buenos Aires

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

Sociedad Argentina de Biología

The mitogen-activated protein kinase (MAPK) signal transduction pathways are known to be involved in various processes of growth, differentiation and cell death. The purpose of the present study was to examine the roles of ERKs and p38 in cell death induced by Bromocriptine (Bc) in hyperplasic pituitaries. Male Wistar strain rats were estrogenized with estradiol benzoate (15mg) for 30d (E), the last 5d Bc was administered (0,3mg/100g/d) (E+Bc). Control group without treatment (C). Cell death characterization was analyzed by Electron Microscopy. Phosphorylated ERK1/2 (P-ERK) and p38 (P-p38) were detected in cytoplasmic and nuclear fractions by WB. Subcellular localization of these kinases was studied by ICQ at Electron Microscopy level. Statistics: ANOVA-Tukey. The predominant cell death type induced by Bc was a non-apoptotic mechanism characterized by nuclear and cytoplasmic shrinkage, striking vacuolization of organelles, compatible with paraptosis. Bc significant increased (p<0,05 vs C and E) P-ERK and P-p38 expression in nuclear fraction. Bromocriptine induced an intense immunogold labelling for P-p38 and P-ERK1/2 at nuclear level in pituitary cells.