17b-ESTRADIOL ABROGATES APOPTOSIS IN THE C2C12 MUSCLE CELL LINE THROUGH NON- CLASICAL ESTROGEN RECEPTORS

VASCONSUELO, A; MILANESI, L; BOLAND, R

Pinamar

Congreso; XLI Reunión Anual de la Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular - SAIB; 2005

The action of estrogen can be mediated by the classical nuclear estrogen receptor or through putative receptors with non-classical localization. There are evidences showing antiapototic effects of estradiol in various cell classes. The present study was aimed to analyze these effects of 17b-estradiol in apoptotic murine skeletal muscle C2C12 cells. We demonstrated by DAPI staining, DNA laddering and Western blot assays using anti-PARP antibody that etoposide (25 mg/ml), as well as H2O2 (1 mM), induced apoptosis which was inhibited by estradiol. In contrast, The estradiol-BSA conjugate did not exert this protective effect. Apoptosis was not inhibited by estradiol using saponin-permeabilized C2C12 cells in presence of a monoclonal anti-ERa antibody against the ER estradiol binding domain. In view that immunocytochemistry and ligand binding  studies indicate that the ER is mainly localized in  mitochondria, and that 17b-estradiol treatment does not translocate ER to the nucleus, the antiapototic action of  estradiol in C2C12 muscle cells may involve the activation of  non-classically located estradiol receptors.