Increased expression of the putative axon growth-repulsive extracellular matrix molecule, keratan sulphate proteoglycan, following traumatic injury of the adult rat spinal cord.
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 axons 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.
Krautstrunk
M
M
Department of Neurology, Aachen University Medical School, RWTH Aachen, Pauwelsstrasse 30, 52057 Aachen, Germany.
Scholtes
F
F
Martin
D
D
Schoenen
J
J
Schmitt
A B
AB
Plate
D
D
Nacimiento
W
W
Noth
J
J
Brook
G A
GA
D000818:Animals; D001369:Axons / Q000187:drug effects* / Q000276:immunology / Q000473:pathology*; D011508:Chondroitin Sulfate Proteoglycans / Q000032:analysis* / Q000276:immunology; D004195:Disease Models, Animal; D016326:Extracellular Matrix Proteins / Q000032:analysis* / Q000276:immunology; D007632:Keratan Sulfate / Q000032:analysis* / Q000276:immunology; D000071234:Lumican; D008297:Male; D009416:Nerve Regeneration / Q000187:drug effects* / Q000276:immunology; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000276:immunology / Q000473:pathology*; D013997:Time Factors
D011508:Chondroitin Sulfate Proteoglycans; D016326:Extracellular Matrix Proteins; C000604308:Lum protein, rat; D000071234:Lumican; D007632:Keratan Sulfate