info:eu-repo/semantics/article
17β-estradiol abrogates apoptosis in murine skeletal muscle cells through estrogen receptors: Role of the phosphatidylinositol 3-kinase/Akt pathway
Fecha
2008-02Registro en:
Vasconsuelo, Andrea Anahi; Milanesi, Lorena Magdalena; Boland, Ricardo Leopoldo; 17β-estradiol abrogates apoptosis in murine skeletal muscle cells through estrogen receptors: Role of the phosphatidylinositol 3-kinase/Akt pathway; BioScientifica; Journal of Endocrinology; 196; 2; 2-2008; 385-397
0022-0795
CONICET Digital
CONICET
Autor
Vasconsuelo, Andrea Anahi
Milanesi, Lorena Magdalena
Boland, Ricardo Leopoldo
Resumen
Estrogens can regulate apoptosis in various cellular systems. The present study shows that 17β-estradiol (E2), at physiological concentrations, abrogates DNA damage, poly (ADP-ribose) polymerase cleavage, and mitochondrial cytochrome c release induced by H2O2 or etoposide in mouse skeletal muscle C2C12 cells. This protective action, which involved P13K/Akt activation and Bcl-2 associated death agonist (BAD) phosphorylation, was inhibited by antibodies against the estrogen receptor (ER) α or β isoforms, or transfecting siRNA specific for each isoform. The inhibition of the antiapoptotic action of E2 at the mitochondrial level was more pronounced when ER-β was immunoneutralized or suppressed by mRNA silencing, whereas transfection of C2C12 cells with either ER-α siRNA or ER-β siRNA blocked the activation of Akt by E2, suggesting differential involvement of ER isoforms depending on the step of the apoptotic/survival pathway evaluated. These results indicate that E2 exerts antiapoptotic effects in skeletal muscle cells which are mediated by ER-β and ER-α and involve the PI3K/Akt pathway.