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Title: CCAAT/Enhancer binding protein β silencing mitigates glial activation and neurodegeneration in a rat model of Parkinson's disease.
Authors: Morales-Garcia, Jose A
Gine, Elena
Hernandez-Encinas, Elena
Aguilar-Morante, Diana
Sierra-Magro, Ana
Sanz-SanCristobal, Marina
Alonso-Gil, Sandra
Sanchez-Lanzas, Raul
Castaño, Jose G
Santos, Angel
Perez-Castillo, Ana
metadata.dc.subject.mesh: Animals
CCAAT-Enhancer-Binding Protein-beta
Cells, Cultured
Disease Models, Animal
Dopaminergic Neurons
Parkinson Disease
Pars Compacta
RNA Interference
RNA, Small Interfering
Rats, Wistar
Issue Date: 19-Oct-2017
Abstract: 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.
metadata.dc.identifier.doi: 10.1038/s41598-017-13269-4
Appears in Collections:Producción 2020

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