Reference : Increased expression of the putative axon growth-repulsive extracellular matrix molecule...
Scientific journals : Article
Human health sciences : Surgery
Social & behavioral sciences, psychology : Neurosciences & behavior
Human health sciences : Neurology
http://hdl.handle.net/2268/7220
Increased expression of the putative axon growth-repulsive extracellular matrix molecule, keratan sulphate proteoglycan, following traumatic injury of the adult rat spinal cord
English
Krautstrunk, M. [> > > >]
Scholtes, Félix mailto [Université de Liège - ULg > Département des sciences cliniques > Neurochirurgie >]
Martin, Didier mailto [Université de Liège - ULg > Département des sciences cliniques > Neurochirurgie]
Schoenen, Jean mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Neuro-anatomie]
Schmitt, A. B. [> > > >]
Plate, D. [> > > >]
Nacimiento, W. [> > > >]
Noth, J. [> > > >]
Brook, G. A. [> > > >]
Dec-2002
Acta Neuropathologica
Springer-Verlag
104
6
592-600
Yes (verified by ORBi)
International
0001-6322
New York
[en] spinal cord injury ; regeneration ; proteoglycan ; keratan sulphate proteoglycan ; extracellular matrix molecules
[en] Keratan sulphate proteoglycan (KSPG) is a developmentally regulated barrier molecule, directing axonal growth during central nervous system (CNS) formation. The possible re-expression and functional significance of KSPG in preventing axon regeneration following spinal cord injury (SCI) is poorly understood. In the present investigation, the spatio-temporal expression of KSPG was studied following experimental SCI. There was no indication of sparing of axons at the lesion epicentre following severe compression injury. By 7 days post operation (p.o.) a diffuse increase of KSPG immunoreactivity (KSPG-IR) was observed in the parenchyma surrounding the lesion. This was followed by a delayed (21-28 days p.o.) and largely heterogeneous increase of KSPG-IR in the lesion epicentre, which revealed both cellular and extracellular matrix-like distribution patterns. Although no re-growth of anterogradely labelled corticospinal axons was observed, many 200-kDa neurofilament (NF)-positive axon could be detected growing into the connective tissue scar. This phase of spontaneous axonal re-growth was closely associated with a framework of glial cells (including Schwann cells from damaged local spinal nerve roots) that had migrated into the lesion site. The spontaneous nerve fibre re-growth could be detected in both KSPG-rich and KSPG-poor territories. The present data suggest that the lesion-induced up-regulation of KSPG-IR may have contributed to the lack of corticospinal axon re-growth. However, the lack of any direct spatio-temporal correlation between the distribution of raised KSPG-IR and spontaneous NF-positive axonal regeneration suggests that at least some populations of axons can resist the putative inhibitory effects of this extracellular matrix molecule.
http://hdl.handle.net/2268/7220

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