NF-?ÛB activation is involved in tumoural regression process induced by Bromocriptine in pituitary.

PALMERI, C. M.; PETITI, J. P.; SOSA, LV; MUKDSI, J. H.; GUTIERREZ, S.; DE PAUL, A L; TORRES, A I

Congreso; III Iberoamerican Congress of Neuroimmunomodulation; 2009

Previously we demonstrated that Bromocriptine (BC) induces tumor regression mainly by a non-apoptotic cell death also dubbed paraptosis, characterized by cytoplasmic vacuolization on expense to endoplasmic reticulum (ER) and mitochondria swelling. Under stress conditions, the ER initiates pathways signal alarm with NF-£eB activation that requires I£eB£\ dissociation and finally triggers cell suicide. The purpose of the present study was to examine whether NF-£eB is involved in paraptosis induced by BC in hyperplasic pituitaries. Male rats were estrogenized with estradiol benzoate (15mg) for 30d (E), and 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 (EM). NF-£eB and I£eB£\ were detected in cytoplasmic and nuclear fractions by Western Blot. Subcellular localization of NF-£eB was studied by Immunocytochemistry at EM. Statistical analysis: ANOVA-Fisher. In cytoplasmic fractions BC significantly increased NF-£eB expression with a consequent diminution of I£eB£\ (p<0.01 vs. E). At nuclear compartment, BC also induced an augment in NF-£eB expression levels (p<0.01 vs. C and E) that was correlated with an intense immunogold labeling in pituitary cells by EM. These results suggest that BC induced the NF-£eB activation and translocation to nucleus of pituitary cells triggering paraptosis cell death.