JOURNAL ARTICLE

[FGF-2-treatment improves locomotor function via axonal regeneration in the transected rat spinal cord]

Shoei Furukawa, Yoshiko Furukawa
Brain and Nerve, Shinkei Kenkyū No Shinpo 2007, 59 (12): 1333-9
18095482
The failure of axonal regeneration after central nervous system (CNS) injury is thought to be due in part to the expression of molecules inhibitory for axonal growth and/or the lack of neurotrophic factors. Antibody treatment to neutralize axon growth inhibitory activity, and delivery of neurotrophic factor have been attempted extensively to overcome inhibition and augment regeneration of spinal motor pathways. Local delivery of neurotrophins can counteract pathological events and induce a regenerative response after both acute and chronic spinal cord injury. Furthermore, genetically modified cells that deliver neurotrophins, olfactory ensheathing glia that facilitate nerve regeneration and neural stem/progenitor cells that generate neurons or glia have been studied. These experiments result in a substantial level of restoration of motor function, and give evidence for possible regeneration of particular CNS axons related locomotion activity. However, more practical and promising methods to induce more drastic axonal regeneration are desired at present for clinical use. Fibroblast growth factors (FGFs) have been implicated in numerous cellular processes. FGF-2 stimulates the growth of blood vessels via proliferation of endotherial cells and smooth muscle cells, and enhances neurogenesis via mitotic activity of neural stem/progenitor cells. As angiogenesis is crucial for forming nervous system, FGF-2 may play roles for nerve regeneration in the injured spinal cord. We examined the effects on locomotor function of the FGF-2 injected into the completely transected rat spinal cord. The locomotor function of the FGF-2-treated animals was substantially recovered up to extent where the joint of the hind limb moves 6 weeks after transection, but the recovery was not seen at all on the locomotor activity of the vehicle-treated animals. This regeneration might be facilitated by prominant cell growth of fibroblast-like cells markedly enhanced by FGF-2 around the lesion site, because the cells have properties advantageous for neurite outgrowth. FGF-2-induced cells may become a crucial and promising tool to attain successful axonal regeneration.

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