Department of Neuroscience, University of Connecticut Health Center, Farmington, Connecticut 06030, USA.
Brain Res. 2013 Sep 5;1529:39-45. doi: 10.1016/j.brainres.2013.07.030. Epub 2013 Jul 24.
Many neurons degenerate after injuries resulting from overstimulation, drugs, genetic mutations, and aging. Although several growth factors and neurotrophins delay degeneration and promote regrowth of neural processes, the role of fibroblast growth factor 8 (FGF8) in mammalian spiral ganglion neurons (SGN) neurite outgrowth has not been examined. This study develops and uses SGN cell cultures suitable for experimental analysis, it investigates whether FGF8a and FGF8b isoforms affect the neurite outgrowth from SGN cultured in vitro. We found that both FGF8a and FGF8b promoted the outgrowth of neurites from cultured SGN. This response is mediated by FGF receptors and involves the activation of IκBα-mediated NFκB signaling pathway. These findings suggest that, besides its morphogenetic role during development, FGF8 may have trophic functions in the adult which are relevant to regeneration.
许多神经元在过度刺激、药物、基因突变和衰老等导致的损伤后会发生退化。虽然几种生长因子和神经营养因子可以延缓退化并促进神经过程的再生,但成纤维细胞生长因子 8(FGF8)在哺乳动物螺旋神经节神经元(SGN)轴突生长中的作用尚未被研究过。本研究开发并使用了适合实验分析的 SGN 细胞培养物,研究了 FGF8a 和 FGF8b 同工型是否影响体外培养的 SGN 神经元的轴突生长。我们发现,FGF8a 和 FGF8b 都能促进体外培养的 SGN 神经元的轴突生长。这种反应是由 FGF 受体介导的,涉及 IκBα 介导的 NFκB 信号通路的激活。这些发现表明,除了在发育过程中的形态发生作用外,FGF8 在成年期可能具有营养作用,与再生有关。