| First Author | Raivich G | Year | 2004 |
| Journal | Neuron | Volume | 43 |
| Issue | 1 | Pages | 57-67 |
| PubMed ID | 15233917 | Mgi Jnum | J:130619 |
| Mgi Id | MGI:3772001 | Doi | 10.1016/j.neuron.2004.06.005 |
| Citation | Raivich G, et al. (2004) The AP-1 transcription factor c-Jun is required for efficient axonal regeneration. Neuron 43(1):57-67 |
| abstractText | 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. |
