The effects of treatment with antibodies to transforming growth factor beta-1 and beta-2 following spinal cord damage in the adult rat

King, V.R.; Phillips, J.B.; Brown, R.A. and Priestley, J.V. (2004). The effects of treatment with antibodies to transforming growth factor beta-1 and beta-2 following spinal cord damage in the adult rat. Neuroscience, 126(1) pp. 173–183.

DOI: https://doi.org/10.1016/j.neuroscience.2004.03.035

Abstract

We recently showed axonal ingrowth into fibronectin (FN) mats implanted into the spinal cord. However, little axonal growth was found from FN mats into intact spinal cord. Previous research has shown that this is due in part to astrocytosis around an area of CNS damage. Antibodies to transforming growth factor β (TGFβ) can diminish this astrocytosis. TGFβ also has effects on macrophages and Schwann cells, both of which infiltrate the spinal cord following damage. We examined the axonal, Schwann cell, and macrophage infiltration into FN mats as well as the level of astrocytosis and chondroitin sulfate proteoglycan NG2 around FN implants incubated in TGFβ antibodies and implanted into a lesion cavity in the spinal cord. We also examined the effects of applying TGFβ antibodies to a spinal cord hemisection site. Anti-TGFβ1 within FN mats resulted in extensive cavitation, with the area of damage being larger than the original lesion. Cavitation was also seen following application of anti-TGFβ1 to a spinal cord hemisection site. No cavitation was seen following saline, non-immune IgG or anti-TGFβ2 treatment. However, anti-TGFβ2 treatment did result in diminished axonal growth and Schwann cell and macrophage infiltration. Around the implant site, anti-TGFβ2 treatment resulted in a reduction in the level of astrocytosis but had not effect on levels of NG2. Similar effects were seen following anti-TGFβ2 application to spinal cord hemisection sites. The results suggest that anti-TGFβ1 exacerbates secondary damage by preventing the anti-inflammatory effect of endogenous TGFβ1. Anti-TGFβ2 did not enhance axonal regeneration in this model but did slightly reduce astrocytosis.

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