Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide
| cic.isFulltext | SI | |
| cic.isPeerReviewed | true | |
| cic.lugarDesarrollo | Universidad Nacional de La Plata | |
| cic.parentType | Artículo | |
| cic.version | Publicada | |
| dc.date.accessioned | 2023-06-22T18:12:12Z | |
| dc.date.available | 2023-06-22T18:12:12Z | |
| dc.identifier.uri | https://digital.cic.gba.gob.ar/handle/11746/11949 | |
| dc.title | Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide | en |
| dc.type | Artículo | |
| dcterms.abstract | 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. | en |
| dcterms.creator.author | Molinuevo, María Silvina | |
| dcterms.creator.author | Etcheverry, Susana B. | |
| dcterms.creator.author | Cortizo, Ana María | |
| dcterms.identifier.other | DOI:10.1016/j.tox.2005.02.016 | |
| dcterms.identifier.other | ISSN: 1879-3185 | |
| dcterms.identifier.other | ISSN: 0300-483X | |
| dcterms.isPartOf.issue | vol. 210, no. 2-3 | |
| dcterms.isPartOf.series | Toxicology | |
| dcterms.issued | 2005 | |
| dcterms.language | Inglés | |
| dcterms.license | Attribution-NonCommercial-ShareAlike 4.0 International (BY-NC-SA 4.0) | |
| dcterms.subject | Vanadium | en |
| dcterms.subject | NO | en |
| dcterms.subject | Calcium channel | en |
| dcterms.subject | Macrophages | en |
| dcterms.subject | Cytotoxicity | en |
| dcterms.subject.materia | Bioquímica y Biología Molecular |
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