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SUMMARY:Targeting the glial scar to promote repair following spinal cord i
 njury - Dr Elizabeth Bradbury\, King's College London
DTSTART:20130612T151500Z
DTEND:20130612T161500Z
UID:TALK44566@talks.cam.ac.uk
CONTACT:Suzy Blows
DESCRIPTION:One of the many reactive events that occurs following spinal c
 ord injury (SCI) is the formation of a glial scar that surrounds the injur
 y site. The glial scar is thought to be an inhibitory barrier to the regro
 wth of injured spinal axons due to the presence of growth inhibitory molec
 ules. Chondroitin sulfate proteoglycans (CSPGs) are one of the main classe
 s of inhibitory molecules that are present in the extracellular matrix of 
 the glial scar\, and are dramatically up-regulated after SCI. The bacteria
 l enzyme chondroitinase ABC (ChABC) removes CSPG glycosaminoglycans\, rend
 ering the SCI environment more permissive to growth\, and is a promising t
 reatment option for SCI. However\, despite the reported beneficial effects
  of ChABC treatment\, the potential for achieving long term efficacy in tr
 aumatic injuries that mimic a human SCI has not yet been realised. Recentl
 y\, a bacterial chondroitinase cDNA has been engineered to allow the expre
 ssion and secretion of active chondroitinase enzyme by mammalian cells. Ge
 ne delivery of ChABC may have a number of advantages compared to previous 
 treatment paradigms\, including sustained delivery by spinal cord cells at
  the site of injury. We have assessed the efficacy of gene delivery of ChA
 BC in a clinically relevant animal model of spinal contusion injury\, whic
 h represents the most common form of SCI in humans. We delivered genetical
 ly modified ChABC via a lentiviral vector (LV-ChABC) to adult rats followi
 ng T10 spinal contusion and have examined changes in spinal injury patholo
 gy and functional outcome. LV-ChABC resulted in sustained and widespread C
 SPG degradation in the contused rat spinal cord and this was associated wi
 th significantly reduced cavitation\, enhanced neuronal survival and spari
 ng of spinal axons\, increased vascularisation throughout the injury site 
 and a marked change in the nature of reactive gliosis and the inflammatory
  response around the injury epicenter and cavity borders. We also describe
  the effects of LV-ChABC on improving spinal conduction and behavioural fu
 nction. These findings identify gene delivery targeting extracellular matr
 ix as a promising strategy for repair following spinal cord injury.
LOCATION:Lecture Theatre 1\, Department of Veterinary Medicine
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