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CCAAT/Enhancer binding protein β silencing mitigates glial activation and neurodegeneration in a rat model of Parkinson’s disease

AuthorsMorales-García, José A. ; Giné, Elena; Hernandez-Encinas, Elena; Aguilar Morante, Diana ; Sierra-Magro, Ana; Sanz-SanCristóbal, Marina ; Alonso-Gil, Sandra ; Sánchez-Lanzas, Raul; Castaño, José G.; Santos, Ángel; Pérez Castillo, Ana
Issue Date2017
PublisherSpringer Nature
CitationScientific Reports 7: 13526 (2017)
AbstractThe 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.
Publisher version (URL)https://doi.org/10.1038/s41598-017-13269-4
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