Enhanced immunoreactivity for basic fibroblast growth factor (FGF2) in the adult rat spinal cord in experimental syringomyelia

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作者
Miyatake, Shin [1 ]
Onodera, Shin [1 ]
Sano, Toshiaki [2 ]
Katoh, Shinsuke [3 ]
Ikata, Takaaki [3 ]
机构
[1] Department of Sports Medicine and Joint Surgery, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
[2] Department of Human Pathology, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima, Japan
[3] Department of Orthopaedics, University of Tokushima Graduate School, Tokushima, Japan
关键词
Fibroblasts - Cell membranes - Cell culture;
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摘要
This study design is experimental study using a syringomyelia model. Fibroblast growth factor (FGF) 2 is an endogenous neurotrophic growth factor in the central nervous system (CNS). The aim of this study was to examine how the spatial and temporal expression of FGF2 in the rat spinal cord changes over the 20-week period following the induction of experimental syringomyelia in rats. Rats were subjected to intracisternal injection of kaolin, which causes syringomyelia. The rats were sacrificed at 0, 3, 7, 10, and 12 weeks, and the spinal cord was histologically examined. The localization of FGF-2 and glial fibrillary acidic protein (GFAP) was also examined by immunohistochemistry. In the normal, slight FGF2 immunoreactivity was observed in a few axons and myelin sheaths in the white matter of the spinal cord. Three weeks after injection, no syrinx formation and little vacuolar degeneration were seen in the white matter, while a mild increase in FGF2 immunoreactivity were in some axons and myelin sheaths. At 7, 10, and 20 weeks, the central canal and the syrinx formation were enlarged. These changes were followed by demyelination. The number of FGF2-positive axons and myelin sheaths increased over time, and this seemed to correlate positively with the progress of the vacuolar degenerative changes. These results showed a detailed expression pattern of FGF2 during the establishment process of experimental syringomyelia, and suggest that a role played by FGF2 in the pathophysiology of this disease.
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页码:167 / 175
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