STAT3 promotes corticospinal remodelling and functional recovery after spinal cord injury.
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.
Institute of Clinical Neuroimmunology, Ludwig-Maximilians Universität, Marchioninistrasse 17, Munich 81377, Germany.
Claudia
C
Lang
Peter M
PM
Bradley
Anne
A
Jacobi
Martin
M
Kerschensteiner
Florence M
FM
Bareyre
D000818:Animals; D017353:Gene Deletion; D051379:Mice; D008810:Mice, Inbred C57BL; D009416:Nerve Regeneration; D009474:Neurons / Q000378:metabolism; D011712:Pyramidal Tracts / Q000378:metabolism / Q000502:physiology*; D050796:STAT3 Transcription Factor / Q000235:genetics / Q000378:metabolism*; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology
D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse