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Examinando Artículos y presentaciones en Congresos por Autor "Bruzzone, Liliana"
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Acceso Abierto Osteogenic activity of vanadyl(IV)–ascorbate complex: evaluation of its mechanism of action(2006) Cortizo, Ana María; Molinuevo, M. Silvina; Barrio, Daniel A.; Bruzzone, LilianaWe have previously shown that different vanadium(IV) complexes regulate osteoblastic growth. Since vanadium compounds are accumulated in vivo in bone, they may affect bone turnover. The development of vanadium complexes with different ligands could be an alternative strategy of use in skeletal tissue engineering. In this study, we have investigated the osteogenic properties of a vanadyl(IV)–ascorbate (VOAsc) complex, as well as its possible mechanisms of action, on two osteoblastic cell lines in culture. VOAsc (2.5–25 M) significantly stimulated osteoblastic proliferation (113–125% basal, p < 0.01) in UMR106 cells, but not in the MC3T3E1 cell line. VOAsc (5–100 M) dose-dependently stimulated type-I collagen production (107–156% basal) in osteoblasts. After 3 weeks of culture, 5–25 M VOAsc increased the formation of nodules of mineralization in MC3T3E1 cells (7.7–20-fold control, p < 0.001). VOAsc (50–100 M) significantly stimulated apoptosis in both cell lines (170–230% basal, p < 0.02–0.002), but did not affect reactive oxygen species production. The complex inhibited alkaline and neutral phosphatases from osteoblastic extracts with semi-maximal effect at 10 M doses. VOAsc induced the activation and redistribution of P-ERK in a time- and dose-dependent manner. Inhibitors of the mitogen activated protein kinases (MAPK) pathway (PD98059 and UO126) partially blocked the VOAsc-enhanced osteoblastic proliferation and collagen production. In addition, wortmanin, a PI-3-K inhibitor and type-L channel blocker nifedipine also partially abrogated these effects of VOAsc on osteoblasts. Our in vitro results suggest that this vanadyl(IV)–ascorbate complex could be a useful pharmacological tool for bone tissue regeneration. - Artículo
Acceso Abierto A possible role of oxidative stress in the vanadium-induced cytotoxicity in the MC3T3E1 osteoblast and UMR106 osteosarcoma cell lines(2016) Cortizo, Ana María; Bruzzone, Liliana; Molinuevo, Silvina; Etcheverry, Susana BeatrizThe cytotoxicity and free radical production induced by vanadium compounds were investigated in an osteoblast (MC3T3E1) and an osteosarcoma (UMR106) cell lines in culture. Vanadate induced cell toxicity, reactive oxygen species (ROS) formation and thiobarbituric acid reactive substances (TBARS) increased in a concentration-dependent manner (0.1–10 mM) after 4 h. The concentration–response curve of vanadate-induced cytotoxicity and oxidative stress in MC3T3E1 cells was shifted to the left of the UMR106 curve, suggesting a greater sensitivity of the non-transformed cells in comparison to the osteosarcoma UMR106 cells. Supplementing with vitamin E acetate (80 mM) significantly inhibited ROS and TBARS formation but did not improve the vanadate-dependent decrease in cell number. Other vanadium compounds (vanadyl, pervanadate, and VO:Aspi, a complex of vanadyl(IV) with aspirin) showed different degrees of cell toxicity and induced oxidative stress. Altogether these results suggest that oxidative stress is involved in vanadium induced osteoblastic cytotoxicity, although the mechanism is unknown. © 2000 Elsevier Science Ireland Ltd. All rights reserved.