Artículos de revistas
Antioxidant defense and apoptotic effectors in ascorbic acid and beta-glycerophosphate-induced osteoblastic differentiation
Registro en:
Development Growth & Differentiation. Wiley-blackwell Publishing, Inc, v. 53, n. 1, n. 88, n. 96, 2011.
0012-1592
WOS:000286597800010
10.1111/j.1440-169X.2010.01232.x
Autor
Neto, AHC
Machado, D
Yano, CL
Ferreira, CV
Institución
Resumen
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) MC3T3-E1 cells grown in the presence of ascorbic acid and beta-glycerophosphate (AA/beta-GP) express alkaline phosphatase and produce an extensive collagenous extracellular matrix. Differentiated MC3T3-E1 cells are more sensitive to hydrogen peroxide-induced oxidative stress than undifferentiated cells. In this study, we compared the profile of antioxidant enzymes and molecular markers of apoptosis in undifferentiated and differentiated MC3T3-E1 cells (cell differentiation was induced by treatment with AA/beta-GP). Differentiated osteoblasts showed lower expression and activity of catalase, glutathione S-transferase and glutathione peroxidase. The total superoxide dismutase activity and the expression of Cu/Zn superoxide dismutase were also lower, while the expression of Mn superoxide dismutase was higher in differentiated osteoblasts. The level of malondialdehyde, a widely used marker for oxidative stress, was lower in the AA/beta-GP group compared with control cells, but this difference was not significant. Western blotting showed that treatment with AA/beta-GP increased the Bax/Bcl-2 ratio used as an index of cellular vulnerability to apoptosis. In addition, the activities of caspases 3, 8 and 9 and cleaved poly (ADP) ribose polymerase were significantly higher in differentiated cells. These findings provide new insights into how changes in the activities of major antioxidant enzymes and in the signaling pathways associated with apoptosis may influence the susceptibility of bone cells to oxidative stress. 53 1 88 96 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) FAPESP [06/00430-1]