Fibroblast growth factor-2 (FGF-2) is a pleiotropic cytokine with both in-vivo and in-vitro neurotrophic and gliogenic properties. In the brain, it is localized to astrocytes and discrete neuronal populations. Acting through FGF receptor 1, FGF-2 plays a prominent role in the regulation of central nervous system injury responses, which include the transformation of reactive astrocytes, scar formation, neurogenesis and the promotion of neurotrophic activities.Aim of the work
The aim of the present study was to investigate the cellular mechanisms underlying the restorative actions of FGF-2, and to analyse the changes within astroglial cells in greater detail.Materials and methods
The spinal cord was exposed and crushed with fine forceps in four regions: the brain stem, and the anterior, middle and posterior parts of the spinal cord. Samples of the spinal cord were obtained at intervals of 1, 2 and 6 weeks, snap-frozen in liquid nitrogen and stored at −80°C. Immunohistochemical methods were used to localize FGF-2 and glial fibrillary acidic protein.Results
Spinal cord injuries trigger a significant increase in FGF-2 immunoreactivity and reactive astrocytes at the sites of insult in the brain stem and in the middle and posterior regions, but not in the anterior region, of the spinal cord. The increase in FGF-2 was accompanied by an increase in glial fibrillary acidic protein immunoreactivity in the brain stem and in the middle and posterior regions. These results were recorded in comparison with sham-operated cases in the brain stem and in the middle and posterior regions. In addition, these results were time-dependent.Conclusion
Spinal cord injuries trigger a significant increase in FGF-2 immunoreactivity and reactive astrocytes at the sites of insult except in the anterior region of the spinal cord. The increase in FGF-2 was accompanied by an increase in GFAP immunoreactivity, and the results were time-dependent.