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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-1957

Raivich, G; Bohatschek, M; Da Costa, C; Iwata, O; Galiano, M; Hristova, M; Nateri, A S; Makwana, M; Riera-Sans, L; Wolfer, D P; Lipp, H P; Aguzzi, A; Wagner, E F; Behrens, A (2004). The AP-1 transcription factor c-Jun is required for efficient axonal regeneration. Neuron, 43(1):57-67.

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Abstract

Nerve injury triggers numerous changes in the injured neurons and surrounding nonneuronal cells that ultimately result in successful target reinnervation or cell death. c-Jun is a component of the heterodimeric AP-1 transcription factor, and c-Jun is highly expressed in response to neuronal trauma. Here we have investigated the role of c-jun during axonal regeneration using mice lacking c-jun in the central nervous system. After transection of the facial nerve, the absence of c-Jun caused severe defects in several aspects of the axonal response, including perineuronal sprouting, lymphocyte recruitment, and microglial activation. c-Jun-deficient motorneurons were atrophic, resistant to axotomy-induced cell death, and showed reduced target muscle reinnervation. Expression of CD44, galanin, and alpha7beta1 integrin, molecules known to be involved in regeneration, was greatly impaired, suggesting a mechanism for c-Jun-mediated axonal growth. Taken together, our results identify c-Jun as an important regulator of axonal regeneration in the injured central nervous system.

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205 citations in Web of Science®
219 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:8 July 2004
Deposited On:11 Feb 2008 12:26
Last Modified:27 Nov 2013 19:31
Publisher:Elsevier
ISSN:0896-6273
Publisher DOI:10.1016/j.neuron.2004.06.005
PubMed ID:15233917

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