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成纤维细胞生长因子-2基因的靶向破坏会影响对周围神经损伤的反应。

Targeted disruption of the FGF-2 gene affects the response to peripheral nerve injury.

作者信息

Jungnickel Julia, Claus Peter, Gransalke Kathleen, Timmer Marco, Grothe Claudia

机构信息

Department of Neuroanatomy OE 4140, Center of Anatomy, Hannover Medical School, D-30623 Hannover, Germany.

出版信息

Mol Cell Neurosci. 2004 Mar;25(3):444-52. doi: 10.1016/j.mcn.2003.11.007.

DOI:10.1016/j.mcn.2003.11.007
PMID:15033172
Abstract

Basic fibroblast growth factor (FGF-2) is involved in the development, maintenance, and survival of the nervous system. To study the physiological role of endogenous FGF-2 during peripheral nerve regeneration, we analyzed sciatic nerves of FGF-2-deleted mice by using morphometric, morphological, and immunocytochemical methods. Quantification of number and size of myelinated axons in intact sciatic nerves revealed no difference between wild-type and FGF-2 knock-out (ko) animals. One week after nerve crush, FGF-2 ko mice showed about five times more regenerated myelinated axons with increased myelin and axon diameter in comparison to wild-types close to the injury site. In addition, quantitative distribution of macrophages and collapsed myelin profiles suggested faster Wallerian degeneration in FGF-2-deleted mice close to the lesion site. Our results suggest that endogenous FGF-2 is crucially involved in the early phase of peripheral nerve regeneration possibly by regulation of Schwann cell differentiation.

摘要

碱性成纤维细胞生长因子(FGF - 2)参与神经系统的发育、维持和存活。为研究内源性FGF - 2在周围神经再生过程中的生理作用,我们运用形态测量学、形态学和免疫细胞化学方法分析了FGF - 2基因敲除小鼠的坐骨神经。对完整坐骨神经中有髓轴突的数量和大小进行定量分析,结果显示野生型和FGF - 2基因敲除(ko)动物之间并无差异。神经挤压一周后,与损伤部位附近的野生型小鼠相比,FGF - 2基因敲除小鼠的再生有髓轴突数量多出约五倍,且髓鞘和轴突直径增大。此外,巨噬细胞的定量分布和崩解的髓鞘轮廓表明,在损伤部位附近,FGF - 2基因敲除小鼠的华勒氏变性更快。我们的研究结果表明,内源性FGF - 2可能通过调节雪旺细胞分化,在周围神经再生的早期阶段发挥关键作用。

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