Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide
- Autores
- Molinuevo, María Silvina; Etcheverry, Susana B.; Cortizo, Ana María
- Año de publicación
- 2005
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- 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.
- Materia
-
Bioquímica y Biología Molecular
Vanadium
NO
Calcium channel
Macrophages
Cytotoxicity - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by-nc-sa/4.0/
- Repositorio
.jpg)
- Institución
- Comisión de Investigaciones Científicas de la Provincia de Buenos Aires
- OAI Identificador
- oai:digital.cic.gba.gob.ar:11746/11949
Ver los metadatos del registro completo
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Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxideMolinuevo, María SilvinaEtcheverry, Susana B.Cortizo, Ana MaríaBioquímica y Biología MolecularVanadiumNOCalcium channelMacrophagesCytotoxicityBone 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.2005info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://digital.cic.gba.gob.ar/handle/11746/11949enginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.tox.2005.02.016info:eu-repo/semantics/altIdentifier/issn/1879-3185info:eu-repo/semantics/altIdentifier/issn/0300-483Xinfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/reponame:CIC Digital (CICBA)instname:Comisión de Investigaciones Científicas de la Provincia de Buenos Airesinstacron:CICBA2025-10-23T11:14:21Zoai:digital.cic.gba.gob.ar:11746/11949Institucionalhttp://digital.cic.gba.gob.arOrganismo científico-tecnológicoNo correspondehttp://digital.cic.gba.gob.ar/oai/snrdmarisa.degiusti@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:94412025-10-23 11:14:21.551CIC Digital (CICBA) - Comisión de Investigaciones Científicas de la Provincia de Buenos Airesfalse |
| dc.title.none.fl_str_mv |
Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide |
| title |
Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide |
| spellingShingle |
Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide Molinuevo, María Silvina Bioquímica y Biología Molecular Vanadium NO Calcium channel Macrophages Cytotoxicity |
| title_short |
Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide |
| title_full |
Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide |
| title_fullStr |
Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide |
| title_full_unstemmed |
Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide |
| title_sort |
Macrophage activation by a vanadyl–aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide |
| dc.creator.none.fl_str_mv |
Molinuevo, María Silvina Etcheverry, Susana B. Cortizo, Ana María |
| author |
Molinuevo, María Silvina |
| author_facet |
Molinuevo, María Silvina Etcheverry, Susana B. Cortizo, Ana María |
| author_role |
author |
| author2 |
Etcheverry, Susana B. Cortizo, Ana María |
| author2_role |
author author |
| dc.subject.none.fl_str_mv |
Bioquímica y Biología Molecular Vanadium NO Calcium channel Macrophages Cytotoxicity |
| topic |
Bioquímica y Biología Molecular Vanadium NO Calcium channel Macrophages Cytotoxicity |
| dc.description.none.fl_txt_mv |
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. |
| description |
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. |
| publishDate |
2005 |
| dc.date.none.fl_str_mv |
2005 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
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publishedVersion |
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https://digital.cic.gba.gob.ar/handle/11746/11949 |
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https://digital.cic.gba.gob.ar/handle/11746/11949 |
| dc.language.none.fl_str_mv |
eng |
| language |
eng |
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info:eu-repo/semantics/altIdentifier/doi/10.1016/j.tox.2005.02.016 info:eu-repo/semantics/altIdentifier/issn/1879-3185 info:eu-repo/semantics/altIdentifier/issn/0300-483X |
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openAccess |
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application/pdf |
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