Sapieha Przemyslaw S, Hauswirth William W, Di Polo Adriana
Department of Pathology and Cell Biology, Université de Montréal, Montreal, Quebec, Canada.
J Neurosci Res. 2006 May 1;83(6):985-95. doi: 10.1002/jnr.20803.
The intracellular signaling mechanisms used by neurotrophic factors to promote axon growth in the mature, injured central nervous system are not well understood. Here we investigated the signaling cascades that control fibroblast growth factor-2 (FGF-2)-mediated retinal ganglion cell (RGC) axon extension in vivo. For this purpose, a novel adeno-associated virus (AAV) was used to deliver the FGF-2 gene to RGCs, providing a sustained source of this neurotrophic factor. FGF-2 gene transfer led to an approximately ten-fold increase in the number of axons that extended past the lesion site compared with control nerves. Axon growth correlated with FGF-2-induced activation of the extracellular signal-regulated kinases 1/2 (Erk1/2), but not phosphoinositide 3-kinase or protein kinase C. Pharmacological inhibition of Erk1/2 activation resulted in an approximately 80% decrease in the number of axons that regenerated in the injured optic nerve. Our data demonstrate that the Erk1/2 pathway is an essential signaling component in FGF-2-mediated axon regeneration in the mature, injured visual system.
神经营养因子在成熟的、受损的中枢神经系统中促进轴突生长所使用的细胞内信号传导机制尚未完全明确。在此,我们研究了在体内控制成纤维细胞生长因子2(FGF-2)介导的视网膜神经节细胞(RGC)轴突延伸的信号级联反应。为此,一种新型腺相关病毒(AAV)被用于将FGF-2基因传递给RGC,提供这种神经营养因子的持续来源。与对照神经相比,FGF-2基因转移导致延伸至损伤部位以外的轴突数量增加了约10倍。轴突生长与FGF-2诱导的细胞外信号调节激酶1/2(Erk1/2)的激活相关,但与磷酸肌醇3激酶或蛋白激酶C无关。对Erk1/2激活的药理学抑制导致在受损视神经中再生的轴突数量减少了约80%。我们的数据表明,Erk1/2通路是成熟的、受损的视觉系统中FGF-2介导的轴突再生的重要信号组成部分。