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Conditioning injury-induced spinal axon regeneration requires signal transducer and activator of transcription 3 activation.

Authors: Qiu, J  Cafferty, WB  McMahon, SB  Thompson, SW 
Citation: Qiu J, etal., J Neurosci. 2005 Feb 16;25(7):1645-53.
Pubmed: (View Article at PubMed) PMID:15716400
DOI: Full-text: DOI:10.1523/JNEUROSCI.3269-04.2005

Sensory axons in the adult spinal cord do not regenerate after injury. This is essentially because of inhibitory components in the damaged CNS, such as myelin-associated inhibitors and the glial scar. However, if the sciatic nerve is axotomized before injury of the dorsal column, injured axons can regenerate a short distance in the spinal cord. Here, we show that sciatic nerve transection results in time-dependent phosphorylation and activation of the transcription factor, signal transducer and activator of transcription 3 (STAT3), in dorsal root ganglion (DRG) neurons. This effect is specific to peripheral injuries and does not occur when the dorsal column is crushed. Sustained perineural infusion of the Janus kinase 2 (JAK2) inhibitor AG490 to the proximal nerve stump can block STAT3 phosphorylation after sciatic nerve transection and results in reduced growth-associated protein 43 upregulation and compromised neurite outgrowth in vitro. Importantly, in vivo perineural infusion of AG490 also significantly attenuates dorsal column axonal regeneration in the adult spinal cord after a preconditioning sciatic nerve transection. We conclude that STAT3 activation is necessary for increased growth ability of DRG neurons and improved axonal regeneration in the spinal cord after a conditioning injury.


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CRRD Object Information
CRRD ID: 1641846
Created: 2007-08-23
Species: All species
Last Modified: 2007-08-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.