• Y Goldshmit, F Frisca, J Kaslin, A R Pinto, J-K K Y Tang, A Pébay, R Pinkas-Kramarski, and P D Currie.
• Australian Regenerative Medicine Institute, Monash University, VIC, Australia; Department of Neurobiology, Tel Aviv University, Israel. Electronic address: yona.goldshmit@med.monash.edu.au.
• Neuroscience. 2015 Feb 26;287:104-12.

AbstractPreviously, we have demonstrated a role for fibroblast growth factor (Fgf) in spinal cord regeneration in both zebrafish and mouse. We have shown that exogenous Fgf2 treatment attenuates astrocytic gliosis and induces glia cells to become progenitors that undergo neurogenesis as well as differentiating into bipolar astrocytes that support axonal regeneration (Goldshmit et al., 2012, 2014). One of the downstream signaling target genes of Fgf is spry4, which acts as a feedback inhibitor for Fgf signaling. In this study we examined the effects of increased endogenous Fgf signaling, in spry4-/- mice, on the early events that occur after spinal cord injury (SCI). We demonstrate that in spry4-/- mice inflammatory responses, such as tumor necrosis factor α (TNFα) secretion and macrophage/neutrophil invasion into the lesion site are reduced. In addition, astrocytic gliosis is attenuated and neuronal survival is increased. These results further support a pro-regenerative role of Fgf after SCI, and suggest that increased endogenous Fgf signaling after SCI may contribute to functional recovery and therefore presents this pathway as a target for new therapy development.Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

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