English   español  
Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/112705
Compartir / Impacto:
Estadísticas
Add this article to your Mendeley library MendeleyBASE
Ver citas en Google académico
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar otros formatos: Exportar EndNote (RIS)Exportar EndNote (RIS)Exportar EndNote (RIS)
Título

Phosphodiesterase PDE4B2 expression in an EAE mice model

Autor Sanabra, Cristina; Johansson, Emily ; Martin, Rocío; Mengod Los Arcos, Guadalupe
Fecha de publicación 7-mar-2010
Citación 10th ISNI Congress & 10th ESNI Course (2010)
ResumenInflammatory responses involve cAMP and pharmacological manipulation of cAMP levels by using specific phosphodiesterase (PDE) inhibitors provokes an anti-inflammatory response. Experimental autoimmune encephalomyelitis (EAE) is an animal model of the chronic inflammatory, neurodegenerative demyelinating disease multiple sclerosis (MS). Previously we demonstrated that in the brain and spinal cord of EAE rats there was a dramatic increase in the mRNA expression levels of the PDE4B isoenzyme, solely due to the splicing mRNA variant PDE4B2. This expression was found in the infiltrating T-cells and macrophage/microglia in microvessels and brain parenchyma. We present our results on the alterations in the expression of the cAMP-specific PDE4 and of several inflammatory cytokine mRNAs in the brain and spinal cord of C57BL6 EAE mice model by neuroanatomical techniques (double in situ hybridization histochemistry and immunohistochemistry), and quantitative real time RT-PCR. We observed a PDE4B2 mRNA upregulation after the onset of the EAE model, being significant 30 days post-immunization. No changes on PDE4B3 mRNA splice variant could be detected. Double in situ hybridization and immunohistochemistry studies showed that cellular infiltrates in brain and spinal cord tissues of EAE mice are overexpressing PDE4B isoform. We found that PDE4B2 mRNA splice variant was overexpressed in T cells and macrophages/microglia in the inflammatory foci. These findings support the important and distinctive role of different PDE4 isoforms during the neuroinflammatory response produced by EAE model and its importance as a therapeutic target for the treatment of some neuroinflammatory diseases using subtype-selective PDE4B inhibitors
Descripción Póster presentado en el: !0th ISNI Congress (International Congress of Neuroimmunology) & 10th ESNI Course (European School of NeuroImmunology), celebrado del 26 al 30 de octubre de 2010 en Sitges, Barcelona (España)
Abstract publicado en: Journal of Neurommunology 228(1-2): 49 (2010). DOI 10.1016/j.jneuroim.2010.08.001
URI http://hdl.handle.net/10261/112705
Aparece en las colecciones: (IIBB) Comunicaciones congresos
Ficheros en este ítem:
Fichero Descripción Tamaño Formato  
accesoRestringido.pdf15,38 kBAdobe PDFVista previa
Visualizar/Abrir
Mostrar el registro completo
 


NOTA: Los ítems de Digital.CSIC están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.