Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide
Bone homeostasis is the result of a tight balance between bone resorption and bone formation where macrophage activation is believed to contribute to bone resorption.We have previously shown that a vanadyl(IV)–aspirin complex (VOAspi) regulates cell proliferation and differentiation of osteoblasts i...
| Autores: | , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2005 |
| País: | Argentina |
| Institución: | Comisión de Investigaciones Científicas de la Provincia de Buenos Aires |
| Repositorio: | CIC Digital (CICBA) |
| Idioma: | inglés |
| OAI Identifier: | oai:digital.cic.gba.gob.ar:11746/11949 |
| Acceso en línea: | https://digital.cic.gba.gob.ar/handle/11746/11949 |
| Access Level: | acceso abierto |
| Palabra clave: | Bioquímica y Biología Molecular Vanadium NO Calcium channel Macrophages Cytotoxicity |
| Sumario: | Bone homeostasis is the result of a tight balance between bone resorption and bone formation where macrophage activation is believed to contribute to bone resorption.We have previously shown that a vanadyl(IV)–aspirin complex (VOAspi) regulates cell proliferation and differentiation of osteoblasts in culture. In this study, we assessed VOAspi and VO effects and their possible mechanism of action on a mouse macrophage cell line RAW 264.7. Both vanadium compounds inhibited cell proliferation in a dose-dependent manner. Nifedipine completely reversed the VOAspi-induced macrophage cytotoxicity, while it could not block the effect of VO. VOAspi also stimulated nitric oxide (NO) production, the oxidation of dihydrorhodamine 123 (DHR-123) and enhanced the expression of both constitutive and inducible isoforms of nitric oxide syntases (NOS). All these effects were abolished by nifedipine. Althogether our finding give evidence that VOAspi-induced macrophage cytotoxicity is dependent on L-type calcium channel and the generation of NO though the induction of eNOS and iNOS. Contrary, the parent compound VO exerted a cytotoxic effect by mechanisms independent of a calcium entry and the NO/NOS activation. |
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