In vitro treatment of HepG2 cells with saturated fatty acids reproduces mitochondrial dysfunction found in nonalcoholic steatohepatitis. (Registro nro. 17087)
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| Campo de control de longitud fija | nam a22 7a 4500 |
| 003 - IDENTIFICADOR DEL NÚMERO DE CONTROL | |
| Campo de control | PC17087 |
| 005 - FECHA Y HORA DE LA ÚLTIMA TRANSACCIÓN | |
| Campo de control | 20221124113031.0 |
| 008 - CÓDIGOS DE INFORMACIÓN DE LONGITUD FIJA | |
| Campo de control de longitud fija | 221124b xxu||||| |||| 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) | 1460 |
| Nombre de persona | García Ruiz, Inmaculada |
| Término indicativo de función | Instituto de Investigación i+12 |
| 100 ## - PUNTO DE ACCESO PRINCIPAL - NOMBRE DE PERSONA | |
| 9 (RLIN) | 1461 |
| Nombre de persona | Muñoz Yagüe, María Teresa |
| Término indicativo de función | Aparato Digestivo |
| 100 ## - PUNTO DE ACCESO PRINCIPAL - NOMBRE DE PERSONA | |
| 9 (RLIN) | 514 |
| Nombre de persona | Solís Herruzo, José Antonio |
| Término indicativo de función | Aparato Digestivo |
| 245 00 - MENCIÓN DE TÍTULO | |
| Título | In vitro treatment of HepG2 cells with saturated fatty acids reproduces mitochondrial dysfunction found in nonalcoholic steatohepatitis. |
| Tipo de material | [artículo] |
| 260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT) | |
| Nombre del editor distribuidor etc. | Disease models & mechanisms, |
| Fecha de publicación distribución etc. | 2015 |
| 300 ## - DESCRIPCIÓN FÍSICA | |
| Extensión | 8(2):183-91. |
| 500 ## - NOTA GENERAL | |
| Nota general | Formato Vancouver: García Ruiz I, Solís Muñoz P, Fernández Moreira D, Muñoz Yagüe T, Solís Herruzo JA. In vitro treatment of HepG2 cells with saturated fatty acids reproduces mitochondrial dysfunction found in nonalcoholic steatohepatitis. Dis Model Mech. 2015 Feb;8(2):183-91. |
| 501 ## - NOTA DE “CON” | |
| Nota de "Con" | PMID: 25540128 PMC4314783 |
| 504 ## - NOTA DE BIBLIOGRAFÍA; ETC. | |
| Nota de bibliografía etc. | Contiene 47 referencias |
| 520 ## - NOTA DE SUMARIO; ETC. | |
| Sumario etc. | Activity of the oxidative phosphorylation system (OXPHOS) is decreased in humans and mice with nonalcoholic steatohepatitis. Nitro-oxidative stress seems to be involved in its pathogenesis. The aim of this study was to determine whether fatty acids are implicated in the pathogenesis of this mitochondrial defect. In HepG2 cells, we analyzed the effect of saturated (palmitic and stearic acids) and monounsaturated (oleic acid) fatty acids on: OXPHOS activity; levels of protein expression of OXPHOS complexes and their subunits; gene expression and half-life of OXPHOS complexes; nitro-oxidative stress; and NADPH oxidase gene expression and activity. We also studied the effects of inhibiting or silencing NADPH oxidase on the palmitic-acid-induced nitro-oxidative stress and subsequent OXPHOS inhibition. Exposure of cultured HepG2 cells to saturated fatty acids resulted in a significant decrease in the OXPHOS activity. This effect was prevented in the presence of a mimic of manganese superoxide dismutase. Palmitic acid reduced the amount of both fully-assembled OXPHOS complexes and of complex subunits. This reduction was due mainly to an accelerated degradation of these subunits, which was associated with a 3-tyrosine nitration of mitochondrial proteins. Pretreatment of cells with uric acid, an antiperoxynitrite agent, prevented protein degradation induced by palmitic acid. A reduced gene expression also contributed to decrease mitochondrial DNA (mtDNA)-encoded subunits. Saturated fatty acids induced oxidative stress and caused mtDNA oxidative damage. This effect was prevented by inhibiting NADPH oxidase. These acids activated NADPH oxidase gene expression and increased NADPH oxidase activity. Silencing this oxidase abrogated totally the inhibitory effect of palmitic acid on OXPHOS complex activity. We conclude that saturated fatty acids caused nitro-oxidative stress, reduced OXPHOS complex half-life and activity, and decreased gene expression of mtDNA-encoded subunits. These effects were mediated by activation of NADPH oxidase. That is, these acids reproduced mitochondrial dysfunction found in humans and animals with nonalcoholic steatohepatitis. |
| 710 ## - PUNTO DE ACCESO ADICIONAL - NOMBRE DE ENTIDAD | |
| 9 (RLIN) | 273 |
| Nombre de entidad o nombre de jurisdicción como elemento inicial | Servicio de Medicina del Aparato Digestivo |
| 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/PMC4314783/ |
| Acceso | Acceso libre |
| 942 ## - ENTRADA PARA ELEMENTOS AGREGADOS (KOHA) | |
| Fuente de clasificación o esquema de ordenación en estanterías | |
| Koha [por defecto] tipo de item | Artículo |
| Suprimido en OPAC | Público |
| 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 |
|---|---|---|---|---|---|---|---|---|---|---|---|
| Hospital Universitario 12 de Octubre | Hospital Universitario 12 de Octubre | 2022-11-24 | PC17087 | 2022-11-24 | 2022-11-24 | Artículo |
