N2 Neutrophils, Novel Players in Brain Inflammation After Stroke: Modulation by the PPARγ Agonist Rosiglitazone. [artículo]
Por: Ballesteros, Iván [Instituto de Investigación i+12]
| Cuartero, María Isabel [Instituto de Investigación i+12] | Lizasoain, Ignacio [Instituto de Investigación i+12] | Moraga, Ana [Instituto de Investigación i+12] | Moro, María A [Instituto de Investigación i+12].
Colaborador(es): Instituto de Investigación imas12.
Editor: Stroke, 2013Descripción: 44(12):3498-508.Recursos en línea: Solicitar documento Resumen: BACKGROUND AND PURPOSE: Neutrophils have been traditionally recognized as major mediators of a deleterious inflammatory response in acute ischemic stroke, but their potential as a therapeutic target remains unexplored. Recent evidence indicates that neutrophils may acquire different phenotypes and contribute to resolution of inflammation through the release of anti-inflammatory mediators. Thus, similar to M2 macrophages, neutrophils have been proposed to shift toward an N2 phenotype, a polarization that is peroxisome proliferator-activated receptor-γ dependent in macrophages. We hypothesize that peroxisome proliferator-activated receptor-γ activation with rosiglitazone induces changes in neutrophilic mobilization and phenotype that might influence stroke outcome.
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Artículo
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Formato Vancouver:
Cuartero MI, Ballesteros I, Moraga A, Nombela F, Vivancos J, Hamilton JA et al. N2 neutrophils, novel players in brain inflammation after stroke: modulation by the PPARγ agonist rosiglitazone. Stroke. 2013 Dec;44(12):3498-508.
PMID: 24135932
Contiene 45 referencias
BACKGROUND AND PURPOSE: Neutrophils have been traditionally recognized as major mediators of a deleterious inflammatory response in acute ischemic stroke, but their potential as a therapeutic target remains unexplored. Recent evidence indicates that neutrophils may acquire different phenotypes and contribute to resolution of inflammation through the release of anti-inflammatory mediators. Thus, similar to M2 macrophages, neutrophils have been proposed to shift toward an N2 phenotype, a polarization that is peroxisome proliferator-activated receptor-γ dependent in macrophages. We hypothesize that peroxisome proliferator-activated receptor-γ activation with rosiglitazone induces changes in neutrophilic mobilization and phenotype that might influence stroke outcome.
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