Effect of nitric oxide on mitochondrial activity of human synovial cells (Registro nro. 3991)
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| 000 -CABECERA | |
|---|---|
| Campo de control de longitud fija | 03964na a2200241 4500 |
| 003 - IDENTIFICADOR DEL NÚMERO DE CONTROL | |
| Campo de control | H12O |
| 005 - FECHA Y HORA DE LA ÚLTIMA TRANSACCIÓN | |
| Campo de control | 20210625062801.0 |
| 008 - CÓDIGOS DE INFORMACIÓN DE LONGITUD FIJA | |
| Campo de control de longitud fija | 130622s2011 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 | |
| 9 (RLIN) | 1007 |
| Nombre de persona | Arenas Barbero, Joaquín |
| Término indicativo de función | Instituto de Investigación |
| 100 ## - PUNTO DE ACCESO PRINCIPAL - NOMBRE DE PERSONA | |
| 9 (RLIN) | 345 |
| Nombre de persona | Martín Casanueva, Miguel Ángel |
| Término indicativo de función | Bioquímica Clínica |
| 245 00 - MENCIÓN DE TÍTULO | |
| Título | Effect of nitric oxide on mitochondrial activity of human synovial cells |
| Tipo de material | [artículo] |
| 260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT) | |
| Nombre del editor distribuidor etc. | BMC Musculoskeletal Disorders, |
| Fecha de publicación distribución etc. | 2011 |
| 300 ## - DESCRIPCIÓN FÍSICA | |
| Extensión | 12:42. |
| 500 ## - NOTA GENERAL | |
| Nota general | Formato Vancouver: Cillero-Pastor B, Martin MA, Arenas J, López-Armada MJ, Blanco FJ. Effect of nitric oxide on mitochondrial activity of human synovial cells. BMC Musculoskelet Disord. 2011;12:42. |
| 501 ## - NOTA DE “CON” | |
| Nota de "Con" | PMID: 21303534 |
| 504 ## - NOTA DE BIBLIOGRAFÍA; ETC. | |
| Nota de bibliografía etc. | Contiene 42 referencias |
| 520 ## - NOTA DE SUMARIO; ETC. | |
| Sumario etc. | BACKGROUND: Nitric oxide (NO) is a messenger implicated in the destruction and inflammation of joint tissues. Cartilage and synovial membrane from patients with rheumatoid arthritis (RA) and osteoarthritis (OA) have high levels of NO. NO is known to modulate various cellular pathways and, thus, inhibit the activity of the mitochondrial respiratory chain (MRC) of chondrocytes and induce the generation of reactive oxygen species (ROS) and cell death in multiple cell types. For these reasons, and because of the importance of the synovial membrane in development of OA pathology, we investigated the effects of NO on survival, mitochondrial function, and activity of fibroblastic human OA synovial cells. METHODS: Human OA synovia were obtained from eight patients undergoing hip joint replacement. Sodium nitroprusside (SNP) was used as a NO donor compound and cell viability was evaluated by MTT assays. Mitochondrial function was evaluated by analyzing the mitochondrial membrane potential (Δψm) with flow cytometry using the fluorofore DePsipher. ATP levels were measured by luminescence assays, and the activities of the respiratory chain complexes (complex I: NADH CoQ₁ reductase, complex II: succinate dehydrogenase, complex III: ubiquinol-cytochrome c reductase, complex IV: cytochrome c oxidase) and citrate synthase (CS) were measured by enzymatic assay. Protein expression analyses were performed by western blot. RESULTS: SNP at a concentration of 0.5 mM induced cell death, shown by the MTT method at different time points. The percentages of viable cells at 24, 48 and 72 hours were 86.11 ± 4.9%, 74.31 ± 3.35%, and 43.88 ± 1.43%, respectively, compared to the basal level of 100% (*p < 0.05). SNP at 0.5 mM induced depolarization of the mitochondrial membrane at 12 hours with a decrease in the ratio of polarized cells (basal = 2.48 ± 0.28; SNP 0.5 mM = 1.57 ± 0.11; *p < 0.01). The time course analyses of treatment with SNP at 0.5 mM demonstrated that treatment reliably and significantly reduced intracellular ATP production (68.34 ± 14.3% vs. basal = 100% at 6 hours; *p < 0.05). The analysis of the MRC at 48 hours showed that SNP at 0.5 mM increased the activity of complexes I (basal = 36.47 ± 3.92 mol/min/mg protein, SNP 0.5 mM = 58.08 ± 6.46 mol/min/mg protein; *p < 0.05) and III (basal = 63.87 ± 6.93 mol/min/mg protein, SNP 0.5 mM = 109.15 ± 30.37 mol/min/mg protein; *p < 0.05) but reduced CS activity (basal = 105.06 ± 10.72 mol/min/mg protein, SNP at 0.5 mM = 66.88 ± 6.08 mol/min/mg protein.; *p < 0.05), indicating a decrease in mitochondrial mass. Finally, SNP regulated the expression of proteins related to the cellular cycle; the NO donor decreased bcl-2, mcl-1 and procaspase-3 protein expression. CONCLUSIONS: This study suggests that NO reduces the survival of OA synoviocytes by regulating mitochondrial functionality, as well as the proteins controlling the cell cycle. |
| 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) | http://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/1471-2474-12-42 |
| 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 | Identificador uniforme del recurso | Fecha del precio de reemplazo | Tipo de item de Koha |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Hospital Universitario 12 de Octubre | Hospital Universitario 12 de Octubre | 2016-01-21 | PC3991 | 2016-01-21 | http://opac.h12o.es/pdf/pc/3/pc3991.pdf | 2016-01-21 | Artículo |
