Increased TGFbeta1 and TGFbeta2 expression following spinal cord injury in rats

Transforming growth factor-betas (TGFbetas) are implicated in fibrotic pathologies. TGFbeta1 and -beta2 expression is increased around the glial/fibrotic scar in the injured brain. Moreover, local injection of TGFbeta3 antagonists into cerebral wounds reduces glial scarring. Here, we monitored expression of TGFbeta1 and -beta2 mRNA and protein in the spinal cord after transection of the dorsal funiculi. Levels of TGFbeta1 mRNA were most elevated over the acute inflammatory phase, while TGFbeta2 mRNA levels were raised locally about the wound, particularly in astrocytes and neovascular endothelial cells, over the subacute period of scarring. TGFbeta3 protein production also increased after injury. Both TGFbeta1 and TGFbeta2 were found in hematogenous inflammatory cells, while TGFbeta1 was also neuronassociated, and high levels of TGFbeta2 were localized to multiple cell types in the wound, including reactive astrocytes, during the period of glial/collagen scar formation. The cellular localization and temporal pattern of expression of TGFbeta3 after spinal cord injury suggest that TGFbeta1 modulates the inflammatory and neuronal responses, while TGFbeta2 regulates glial/collagen scarring.