Sapieha Przemyslaw S, Peltier Martin, Rendahl Katherine G, Manning William C, Di Polo Adriana
Department of Pathology and Cell Biology, Université de Montréal, Montreal, Quebec H3T 1J4, Canada.
Mol Cell Neurosci. 2003 Nov;24(3):656-72. doi: 10.1016/s1044-7431(03)00228-8.
Basic fibroblast growth factor (or FGF-2) has been shown to be a potent stimulator of retinal ganglion cell (RGC) axonal growth during development. Here we investigated if FGF-2 upregulation in adult RGCs promoted axon regrowth in vivo after acute optic nerve injury. Recombinant adeno-associated virus (AAV) was used to deliver the FGF-2 gene to adult RGCs providing a sustained source of this neurotrophic factor. FGF-2 gene transfer led to a 10-fold increase in the number of axons that extended past 0.5 mm from the lesion site compared to control nerves. Detection of AAV-mediated FGF-2 protein in injured RGC axons correlated with growth into the distal optic nerve. The response to FGF-2 upregulation was supported by our finding that FGF receptor-1 (FGFR-1) and heparan sulfate (HS), known to be essential for FGF-2 signaling, were expressed by adult rat RGCs. FGF-2 transgene expression led to only transient protection of injured RGCs. Thus the effect of this neurotrophic factor on axon extension could not be solely attributed to an increase in neuronal survival. Our data indicate that selective upregulation of FGF-2 in adult RGCs stimulates axon regrowth within the optic nerve, an environment that is highly inhibitory for regeneration. These results support the hypothesis that key factors involved in axon outgrowth during neural development may promote regeneration of adult injured neurons.
碱性成纤维细胞生长因子(即FGF-2)已被证明在发育过程中是视网膜神经节细胞(RGC)轴突生长的有效刺激物。在此,我们研究了成年RGC中FGF-2的上调是否能促进急性视神经损伤后体内轴突的再生。重组腺相关病毒(AAV)被用于将FGF-2基因传递给成年RGC,从而提供这种神经营养因子的持续来源。与对照神经相比,FGF-2基因转移导致从损伤部位延伸超过0.5毫米的轴突数量增加了10倍。在受损RGC轴突中检测到AAV介导的FGF-2蛋白与向视神经远端的生长相关。我们发现成年大鼠RGC表达FGF受体-1(FGFR-1)和硫酸乙酰肝素(HS),这两者已知对FGF-2信号传导至关重要,这一发现支持了对FGF-2上调的反应。FGF-2转基因表达仅导致对受损RGC的短暂保护。因此,这种神经营养因子对轴突延伸的作用不能仅仅归因于神经元存活率的提高。我们的数据表明,成年RGC中FGF-2的选择性上调刺激了视神经内轴突的再生,而视神经环境对再生具有高度抑制作用。这些结果支持了这样一种假说,即神经发育过程中参与轴突生长的关键因素可能促进成年受损神经元的再生。