ABSTRACT
Penetrating injuries of the central nervous system (CNS) initiate a complex cellular wounding response comprising sequential and overlapping events. The observations of scar formation coinciding with axon growth arrest in the mature CNS provided an early explanation of the aborted regeneration. There is little or no expression of transforming growth factor-ß1 (TGF) in the adult CNS neural parenchyma. Since the foetal and neonatal CNS heals without scarring, one might predict that TGF-ßs would be absent from such wounds. Intraventricular infusion of recombinant TGF-ßs markedly enhances matrix deposition in penetrating CNS wounds. Conversely, local immunoneutralisation of TGF-ß1 and TGF-ß2 activity via intraventricular injections of isoform or pan-specific antibodies into such CNS wounds inhibits mesodermal scarring. TGF-ß1 and TGF-ß2 may act as chemoattractants for blood/meningeal-derived cells, as activators of astrocytes and microglia, and also as potent desmoplastic agents promoting matrix deposition by invading meningeal fibroblasts.
