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dc.contributor.authorMorales-García, José A.es_ES
dc.contributor.authorAguilar Morante, Dianaes_ES
dc.contributor.authorHernandez-Encinas, Elenaes_ES
dc.contributor.authorAlonso-Gil, Sandraes_ES
dc.contributor.authorGil, Carmenes_ES
dc.contributor.authorMartínez, Anaes_ES
dc.contributor.authorSantos, Ángeles_ES
dc.contributor.authorPérez Castillo, Anaes_ES
dc.date.issued2015-02-
dc.identifier.citationNeurobiology of Aging 36(2): 1160–1173 (2015)es_ES
dc.identifier.issn1087-1845-
dc.identifier.urihttp://hdl.handle.net/10261/122641-
dc.description42 p.-10 fig.es_ES
dc.description.abstractDifferent studies have suggested that the nucleotide cyclic adenosine 3’, 5’- monophosphate (cAMP) can actively play an important role as neuroprotective and antiinflammatory agent after a brain injury. The phosphodiesterase 7 (PDE7) enzyme is one of the enzymes responsible for controlling specifically the intracellular levels of cAMP in the immune and central nervous systems. Therefore this enzyme could play an important role in brain inflammation and neurodegeneration. In this regard, using different chemical inhibitors of PDE7 we have demonstrated their neuroprotective and anti-inflammatory activity in different models of neurodegenerative disorders, including Parkinson disease (PD). In the present study, we have used the toxin 6- hydroxydopamine (6-OHDA) and lipopolysaccharide (LPS) to model PD and explore the protective effects of PDE7B deficiency in dopaminergic neurons cell death. Lentivirus-mediated PDE7B deprivation conferred marked in vitro and in vivo neuroprotection against 6-OHDA and LPS toxicity in dopaminergic neurons, and preserved motor function involving the dopamine system in mouse. Our results substantiate previous data and provide a validation of PDE7B enzyme as a valuable new target for therapeutic development in the treatment of PD.es_ES
dc.description.sponsorshipThe authors gratefully acknowledge the financial support of MICINN (Grant SAF2010-16365, to A.P-C and GrantSAF2012-33600, to C.G.). CIBERNED is funded by the Instituto de Salud Carlos III.es_ES
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.relation.isversionofPostprintes_ES
dc.rightsopenAccessen_EN
dc.subjectInflammationes_ES
dc.subjectNew targetes_ES
dc.subjectOxidative stresses_ES
dc.subjectParkinson diseasees_ES
dc.subjectPDE7Bes_ES
dc.subjectshRNAes_ES
dc.titleSilencing phosphodiesterase 7B gene by lentiviral-shRNA interference attenuates neurodegeneration and motor deficits in hemiparkinsonian micees_ES
dc.typeartículoes_ES
dc.identifier.doi10.1016/j.neurobiolaging.2014.10.008-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1016/j.neurobiolaging.2014.10.008es_ES
dc.identifier.e-issn1096-0937-
dc.embargo.terms2016-02es_ES
dc.rights.licensehttp://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.contributor.funderMinisterio de Ciencia e Innovación (España)es_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.contributor.funderCentro Investigación Biomédica en Red Enfermedades Neurodegenerativas (España)-
dc.relation.csices_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004837es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
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