%0 Journal Article
%A Morales-Garcia, Jose A
%A Gine, Elena
%A Hernandez-Encinas, Elena
%A Aguilar-Morante, Diana
%A Sierra-Magro, Ana
%A Sanz-SanCristobal, Marina
%A Alonso-Gil, Sandra
%A Sanchez-Lanzas, Raul
%A Castaño, Jose G
%A Santos, Angel
%A Perez-Castillo, Ana
%T CCAAT/Enhancer binding protein β silencing mitigates glial activation and neurodegeneration in a rat model of Parkinson's disease.
%D 2017
%U http://hdl.handle.net/10668/11703
%X The CCAAT/Enhancer binding protein β (C/EBPβ) is a transcription factor involved in numerous physiological as well as pathological conditions in the brain. However, little is known regarding its possible role in neurodegenerative disorders. We have previously shown that C/EBPβ regulates the expression of genes involved in inflammatory processes and brain injury. Here, we have analyzed the effects of C/EBPβ interference in dopaminergic cell death and glial activation in the 6-hydroxydopamine model of Parkinson's disease. Our results showed that lentivirus-mediated C/EBPβ deprivation conferred marked in vitro and in vivo neuroprotection of dopaminergic cells concomitant with a significant attenuation of the level of the inflammatory response and glial activation. Additionally, C/EBPβ interference diminished the induction of α-synuclein in the substantia nigra pars compacta of animals injected with 6-hydroxydopamine. Taking together, these results reveal an essential function for C/EBPβ in the pathways leading to inflammatory-mediated brain damage and suggest novel roles for C/EBPβ in neurodegenerative diseases, specifically in Parkinson's disease, opening the door for new therapeutic interventions.
%K Neurology
%K Parkinson's disease
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