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.
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.
|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
|Date:||08 July 2004|
|Deposited On:||11 Feb 2008 13:26|
|Last Modified:||27 Nov 2013 20:31|
|Citations:||Web of Science®. Times cited: 188|
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