The Mammalian-Specific Protein Armcx1 Regulates Mitochondrial Transport during Axon Regeneration.
Neuron
; 92(6): 1294-1307, 2016 Dec 21.
Article
en En
| MEDLINE
| ID: mdl-28009275
ABSTRACT
Mitochondrial transport is crucial for neuronal and axonal physiology. However, whether and how it impacts neuronal injury responses, such as neuronal survival and axon regeneration, remain largely unknown. In an established mouse model with robust axon regeneration, we show that Armcx1, a mammalian-specific gene encoding a mitochondria-localized protein, is upregulated after axotomy in this high regeneration condition. Armcx1 overexpression enhances mitochondrial transport in adult retinal ganglion cells (RGCs). Importantly, Armcx1 also promotes both neuronal survival and axon regeneration after injury, and these effects depend on its mitochondrial localization. Furthermore, Armcx1 knockdown undermines both neuronal survival and axon regeneration in the high regenerative capacity model, further supporting a key role of Armcx1 in regulating neuronal injury responses in the adult central nervous system (CNS). Our findings suggest that Armcx1 controls mitochondrial transport during neuronal repair.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Nervio Óptico
/
Células Ganglionares de la Retina
/
Axones
/
Axotomía
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Traumatismos del Nervio Óptico
/
Proteínas Mitocondriales
/
Proteínas del Dominio Armadillo
/
Mitocondrias
/
Regeneración Nerviosa
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Neuron
Asunto de la revista:
NEUROLOGIA
Año:
2016
Tipo del documento:
Article