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J Biol Chem ; 287(38): 31691-702, 2012 Sep 14.
Artículo en Inglés | MEDLINE | ID: mdl-22833673

RESUMEN

Parkinson disease is characterized by the loss of dopaminergic neurons mainly in the substantia nigra. Accumulation of α-synuclein and cell loss has been also reported in many other brain regions including the hippocampus, where it might impair adult neurogenesis, contributing to nonmotor symptoms. However, the molecular mechanisms of these alterations are still unknown. In this report we show that α-synuclein-accumulating adult rat hippocampus neural progenitors present aberrant neuronal differentiation, with reduction of Notch1 expression and downstream signaling targets. We characterized a Notch1 proximal promoter that contains p53 canonical response elements. In vivo binding of p53 represses the transcription of Notch1 in neurons. Moreover, we demonstrated that α-synuclein directly binds to the DNA at Notch1 promoter vicinity and also interacts with p53 protein, facilitating or increasing Notch1 signaling repression, which interferes with maturation and survival of neural progenitors cells. This study provides a molecular basis for α-synuclein-mediated disruption of adult neurogenesis in Parkinson disease.


Asunto(s)
Regulación de la Expresión Génica , Neurogénesis , Neuronas/metabolismo , Enfermedad de Parkinson/metabolismo , Receptor Notch1/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , alfa-Sinucleína/metabolismo , Animales , Apoptosis , Linaje de la Célula , Modelos Animales de Enfermedad , Hipocampo/metabolismo , Lentivirus/genética , Regiones Promotoras Genéticas , Ratas , Transducción de Señal
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