STAT3 promotes corticospinal remodelling and functional recovery after spinal cord injury

被引：75

作者：

Lang, Claudia ^{[1
]}

Bradley, Peter M. ^{[1
]}

Jacobi, Anne ^{[1
]}

Kerschensteiner, Martin ^{[1
,2
]}

Bareyre, Florence M. ^{[1
,2
]}

机构：

[1] Univ Munich, Inst Clin Neuroimmunol, D-81377 Munich, Germany

[2] Munich Cluster Syst Neurol SyNergy, Munich, Germany

来源：

EMBO REPORTS | 2013年 / 14卷 / 10期

基金：

欧洲研究理事会;

关键词：

axonal remodelling; corticospinal tract; neuronal plasticity; spinal cord injury; STAT3; AXONAL PLASTICITY;

D O I：

10.1038/embor.2013.117

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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 de novo 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.

引用

页码：931 / 937

页数：7

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