English   español  
Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/50395
Título

Autophagy promotes survival of retinal ganglion cells after optic nerve axotomy in mice

AutorRodríguez-Muela, N. ; Germain, Francisco; Mariño, G.; Fitze, Patrick S. ; Boya, Patricia
Palabras claveapoptosis
autophagy
neurodegeneration
retina
retinal ganglion cells
Fecha de publicación19-ene-2012
EditorNature Publishing Group
CitaciónCell Death & Differentiation, Jan;19 (1) :162-169 (2012)
ResumenAutophagy is an essential recycling pathway implicated in neurodegeneration either as a pro-survival or a pro-death mechanism. Its role after axonal injury is still uncertain. Axotomy of the optic nerve is a classical model of neurodegeneration. It induces retinal ganglion cell death, a process also occurring in glaucoma and other optic neuropathies. We analyzed autophagy induction and cell survival following optic nerve transection (ONT) in mice. Our results demonstrate activation of autophagy shortly after axotomy with autophagosome formation, upregulation of the autophagy regulator Atg5 and apoptotic death of 50% of the retinal ganglion cells (RGCs) after 5 days. Genetic downregulation of autophagy using knockout mice for Atg4B (another regulator of autophagy) or with specific deletion of Atg5 in retinal ganglion cells, using the Atg5flox/flox mice reduces cell survival after ONT, whereas pharmacological induction of autophagy in vivo increases the number of surviving cells. In conclusion, our data support that autophagy has a cytoprotective role in RGCs after traumatic injury and may provide a new therapeutic strategy to ameliorate retinal diseases
Descripción8 páginas, 5 figuras -- PAGS nros. 162-169
Versión del editorhttp://dx.doi.org/ 10.1038/cdd.2011.88
URIhttp://hdl.handle.net/10261/50395
DOI10.1038/cdd.2011.88
ISSN1350-9047
E-ISSN1476-5403
Aparece en las colecciones: (MNCN) Artículos
(CIB) Artículos
Ficheros en este ítem:
No hay ficheros asociados a este ítem.
Mostrar el registro completo
 

Artículos relacionados:


NOTA: Los ítems de Digital.CSIC están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.