Vanadate-induced nitric oxide production: role in osteoblast growth and differentiation

• Autores: Cortizo, Ana María; Caporossi, Mariana; Lettieri, Gabriela; Etcheverry, Susana B.
• Año de publicación: 2000
• Idioma: español castellano
• Tipo de recurso: artículo
• Materia: Ciencias Químicas; Nitric oxide (NO); Nitric oxide (NO) synthases; Vanadium; Growth; Osteoblast differentiation; Bone; Cytotoxicity
• Institución: Comisión de Investigaciones Científicas de la Provincia de Buenos Aires

Nitric oxide NO. has been shown to act as a mediator of cytokines in bone tissue. We have previously demonstrated that vanadium compounds are insulin- and growth factor-mimetic compounds in osteoblasts in culture, although high doses are toxic to these cells. In this study, we measured NO production in two osteoblast-like cells UMR106 and MC3T3E1. incubated with different concentrations 2.5–100 mM. of vanadate. Vanadate induced NO release in a biphasic manner, with levels being significantly increased at concentrations over 50 mM. The NO donor, sodium nitroprusside, mimicked the vanadate effect: it inhibited cell growth and alkaline phosphatase activity in a dose-dependent manner. Vanadate enhanced the NO synthases, the endothelial and inducible eNOS and iNOS. isoforms, in a dose-dependent manner. Experiments performed with the ionophore A23187 and EGTA suggested that vanadate-induced NO production involves Ca2q-dependent and -independent mechanisms. Altogether, our results suggest that NO may play a critical role in the bioactivity of vanadium in osteoblast-like cells. q2000 Elsevier Science B.V. All rights reserved.