Biblioteca Hospital 12 de Octubre

CCL2/MCP-1 modulation of microglial activation and proliferation (Registro nro. 9491)

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Campo de control de longitud fija 02981na a2200229 4500
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Campo de control H12O
005 - FECHA Y HORA DE LA ÚLTIMA TRANSACCIÓN
Campo de control 20210625062810.0
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Campo de control de longitud fija 130622s2011 xxx||||| |||| 00| 0 eng d
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Centro transcriptor H12O
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Código de lengua del texto/banda sonora o título independiente eng
100 ## - PUNTO DE ACCESO PRINCIPAL - NOMBRE DE PERSONA
Nombre de persona García Bueno, Borja
9 (RLIN) 1897
Término indicativo de función Instituto de Investigación i+12
245 00 - MENCIÓN DE TÍTULO
Título CCL2/MCP-1 modulation of microglial activation and proliferation
Tipo de material [artículo]
260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT)
Nombre del editor distribuidor etc. Journal of Neuroinflammation,
Fecha de publicación distribución etc. 2011
300 ## - DESCRIPCIÓN FÍSICA
Extensión 8:77.
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Nota general Formato Vancouver:
Hinojosa AE, García Bueno B, Leza JC, Madrigal JL. CCL2/MCP-1 modulation of microglial activation and proliferation. J Neuroinflammation. 2011;8:77.
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Nota de "Con" PMID: 21729288
504 ## - NOTA DE BIBLIOGRAFÍA; ETC.
Nota de bibliografía etc. Contiene 51 referencias
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Sumario etc. Monocyte chemoattractant protein (CCL2/MCP-1) is a chemokine that attracts cells involved in the immune/inflammatory response. As microglia are one of the main cell types sustaining inflammation in brain, we proposed here to analyze the direct effects of MCP-1 on cultured primary microglia.
METHODS: Primary microglia and neuronal cultures were obtained from neonatal and embryonic Wistar rats, respectively. Microglia were incubated with different concentrations of recombinant MCP-1 and LPS. Cell proliferation was quantified by measuring incorporation of bromodeoxyuridine (BrdU). Nitrite accumulation was measured using the Griess assay. The expression and synthesis of different proteins was measured by RT-PCR and ELISA. Cell death was quantified by measuring release of LDH into the culture medium.
RESULTS: MCP-1 treatment (50 ng/ml, 24 h) did not induce morphological changes in microglial cultures. Protein and mRNA levels of different cytokines were measured, showing that MCP-1 was not able to induce proinflammatory cytokines (IL-1β, IL6, MIP-1α), either by itself or in combination with LPS. A similar lack of effect was observed when measuring inducible nitric oxide synthase (NOS2) expression or accumulation of nitrites in the culture media as a different indicator of microglial activation. MCP-1 was also unable to alter the expression of different trophic factors that were reduced by LPS treatment. In order to explore the possible release of other products by microglia and their potential neurotoxicity, neurons were co-cultured with microglia: no death of neurons could be detected when treated with MCP-1. However, the presence of MCP-1 induced proliferation of microglia, an effect opposite to that observed with LPS.
CONCLUSION: These data indicate that, while causing migration and proliferation of microglia, MCP-1 does not appear to directly activate an inflammatory response in this cell type, and therefore, other factors may be necessary to cause the changes that result in the neuronal damage commonly observed in situations where MCP-1 levels are elevated.
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://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/9/pc9491.pdf
Acceso Solicitar documento
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Koha [por defecto] tipo de item Artículo
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          Hospital Universitario 12 de Octubre Hospital Universitario 12 de Octubre 2016-01-22 PC9491 2016-01-22 2016-01-22 Artículo

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