STAT3 promotes corticospinal remodelling and functional recovery after spinal cord injury
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- Claudia Lang
- Institute of Clinical Neuroimmunology, Ludwig‐Maximilians Universität Munich 81377 Germany
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- Peter M Bradley
- Institute of Clinical Neuroimmunology, Ludwig‐Maximilians Universität Munich 81377 Germany
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- Anne Jacobi
- Institute of Clinical Neuroimmunology, Ludwig‐Maximilians Universität Munich 81377 Germany
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- Martin Kerschensteiner
- Institute of Clinical Neuroimmunology, Ludwig‐Maximilians Universität Munich 81377 Germany
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- Florence M Bareyre
- Institute of Clinical Neuroimmunology, Ludwig‐Maximilians Universität Munich 81377 Germany
説明
<jats:p>If and how neurons remodel their connections after CNS injury critically influences recovery of function. Here, we investigate the role of the growth‐initiating transcription factor STAT3 during remodelling of the injured corticospinal tract (CST). Endogenous STAT3 expression in lesioned cortical projection neurons is transient but can be sustained by viral gene transfer. Sustained activation of STAT3 enhances remodelling of lesioned CST fibres and induces <jats:italic>de novo</jats:italic> formation of collaterals from unlesioned CST fibres. In a unilateral pyramidotomy paradigm, this recruitment of unlesioned fibres leads to the formation of midline crossing circuits that establish ipsilateral forelimb activation and functional recovery.</jats:p>
収録刊行物
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- EMBO reports
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EMBO reports 14 (10), 931-937, 2013-08-09
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