Nitric oxide compounds have different effects profiles on human articular chondrocyte metabolism. (Registro nro. 13233)
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Campo de control de longitud fija | 02940na a2200229 4500 |
003 - IDENTIFICADOR DEL NÚMERO DE CONTROL | |
Campo de control | PC13233 |
005 - FECHA Y HORA DE LA ÚLTIMA TRANSACCIÓN | |
Campo de control | 20210625062812.0 |
008 - CÓDIGOS DE INFORMACIÓN DE LONGITUD FIJA | |
Campo de control de longitud fija | 130622s2013 xxx||||| |||| 00| 0 eng d |
040 ## - FUENTE DE LA CATALOGACIÓN | |
Centro transcriptor | H12O |
041 ## - CÓDIGO DE LENGUA | |
Código de lengua del texto/banda sonora o título independiente | eng |
100 ## - PUNTO DE ACCESO PRINCIPAL - NOMBRE DE PERSONA | |
Nombre de persona | Arenas Barbero, Joaquín |
9 (RLIN) | 1007 |
Término indicativo de función | Instituto de Investigación |
100 ## - PUNTO DE ACCESO PRINCIPAL - NOMBRE DE PERSONA | |
Nombre de persona | Martín, Miguel A. |
9 (RLIN) | 2412 |
Término indicativo de función | Instituto de Investigación i+12 |
245 00 - MENCIÓN DE TÍTULO | |
Título | Nitric oxide compounds have different effects profiles on human articular chondrocyte metabolism. |
Tipo de material | [artículo] |
260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT) | |
Nombre del editor distribuidor etc. | Arthritis Research & Therapy, |
Fecha de publicación distribución etc. | 2013 |
300 ## - DESCRIPCIÓN FÍSICA | |
Extensión | 15(5):R115. |
500 ## - NOTA GENERAL | |
Nota general | Formato Vancouver: de Andrés MC, Maneiro E, Martín MA, Arenas J, Blanco FJ. Nitric oxide compounds have different effects profiles on human articular chondrocyte metabolism. Arthritis Res Ther. 2013;15(5):R115. |
501 ## - NOTA DE “CON” | |
Nota de "Con" | PMID: 24025112 |
504 ## - NOTA DE BIBLIOGRAFÍA; ETC. | |
Nota de bibliografía etc. | Contiene 63 referencias |
520 ## - NOTA DE SUMARIO; ETC. | |
Sumario etc. | The pathogenesis of osteoarthritis (OA) is characterized by the production of high amounts of nitric oxide (NO), as a consequence of up-regulation of chondrocyte-inducible nitric oxide synthase (iNOS) induced by inflammatory cytokines. NO donors represent a powerful tool for studying the role of NO in the cartilage in vitro. There is no consensus about NO effects on articular cartilage in part because the differences between the NO donors available. The aim of this work is to compare the metabolic profile of traditional and new generation NO donors to see which one points out the osteoarthritic process in the best way. Methods: Human healthy and OA chondrocytes were isolated from patients undergoing joint replacement surgery, and primary cultured. Cells were stimulated with NO donors (NOC-12 or SNP). NO production was evaluated by the Griess method, and apoptosis was quantified by flow cytometry. Mitochondrial function was evaluated by analysing respiratory chain enzyme complexes, citrate synthase (CS) activities by enzymatic assay, mitochondrial membrane potential (Delta psi m) by JC-1 using flow cytometry, and ATP levels were measured by luminescence assays. Glucose transport was measured as the uptake of 2-deoxy-[H-3] lucose (2-[H-3]DG). Statistical analysis was performed using the Mann-Whitney U test. Results: NOC-12 liberates approximately ten times more NO2- than SNP, but the level of cell death induced was not as profound as that produced by SNP. Normal articular chondrocytes stimulated with NOC-12 had reduced activity from complexes I, III y IV, and the mitochondrial mass was increased in these cells. Deleterious effects on Delta psi m and ATP levels were more profound with SNP, and this NO donor was able to reduce 2-[H-3]DG levels. Both NO donors had opposite effects on lactate release, SNP diminished the levels and NOC-12 lead to lactate accumulation. OA chondrocytes incorporate significantly more 2-[H-3]DG than healthy cells. Conclusions: These findings suggest that the new generation donors, specifically NOC-12, mimic the OA metabolic process much better than SNP. Previous results using SNP have to be considered prudently since most of the effects observed can be induced by the interactions of secondary products of NO. |
710 ## - PUNTO DE ACCESO ADICIONAL - NOMBRE DE ENTIDAD | |
9 (RLIN) | 625 |
Nombre de entidad o nombre de jurisdicción como elemento inicial | Instituto de Investigación imas12 |
856 ## - LOCALIZACIÓN Y ACCESO ELECTRÓNICOS | |
Identificador Uniforme del Recurso (URI) | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978712/ |
Acceso | Acceso libre |
942 ## - ENTRADA PARA ELEMENTOS AGREGADOS (KOHA) | |
Suprimido en OPAC | Público |
Fuente de clasificación o esquema de ordenación en estanterías | |
Koha [por defecto] tipo de item | Artículo |
Suprimido | Estado de pérdida | Fuente de clasificación o esquema de ordenación en estanterías | Estropeado | No para préstamo | Localización permanente | Localización actual | Fecha de adquisición | Signatura completa | Fecha última consulta | Fecha del precio de reemplazo | Tipo de item de Koha |
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Hospital Universitario 12 de Octubre | Hospital Universitario 12 de Octubre | 2018-10-26 | PC13223 | 2018-10-26 | 2018-10-26 | Artículo |