Prominent expression of bFGF in dorsal root ganglia after axotomy
Prominent expression of bFGF in dorsal root ganglia after axotomy
复制标题
DOI：
10.1111/j.1460-9568.1995.tb01044.x
复制
发表时间：
1995-12-01
影响因子：
3.4
通讯作者：
Hokfelt, T
中科院分区：
文献类型：
--
作者：
Ji, RR;Zhang, Q;Hokfelt, T
应用定量原位杂交和免疫组织化学方法检测酸性和碱性成纤维细胞生长因子(aFGF、bFGF)在背根节(DRGs)中的表达。在正常背根神经节中，约5%的小神经元表达bFGFm RNA。神经损伤后bFGFm RNA表达显著升高，损伤后3d约80%的DRG神经元表达bFGFm RNA。在轴突切断后15h，bFGF样免疫反应(LI)也明显增加。1周后bFGFm RNA和蛋白水平的升高均下降。切断轴索后，非神经细胞bFGFm RNA表达上调。正常情况下，碱性成纤维细胞生长因子主要定位于背根神经节神经元的胞核和部分非神经元细胞。神经切断后，胞浆内还可见bFGFLI阳性细胞，可见更多bFGF1阳性的非神经细胞。用共聚焦显微镜对切断后的背根节进行分析，发现胞浆内的囊泡状结构和核仁中均可检测到bFGFLI，并可定位于核内。在切断的坐骨神经中应用白血病抑制因子可显著增加bFGF阳性神经元的数量，而非神经元细胞的bFGFLI则受到强烈的抑制。约70%的正常背根节神经元表达aFGFmRNA和aFGFLI。切断中枢神经后，aFGFm RNA水平有一定程度的增加，但对蛋白水平无明显影响。综上所述，本研究结果表明，碱性成纤维细胞生长因子可能参与神经元对损伤的反应，并在轴突切断后的背根节神经元存活和再生中发挥作用。
Using quantitative in situ hybridization and immunohistochemistry the expression of acidic and basic fibroblast growth factors (aFGF, bFGF) in dorsal root ganglia (DRGs) was examined. Around 5% of the small neurons expressed bFGF mRNA in normal DRGs. Nerve injury induced a very dramatic and rapid up-regulation in bFGF mRNA levels, and around 80% of all DRG neurons expressed bFGF mRNA 3 days after axotomy. A distinct increase in bFGF-like immunoreactivity (LI) was also detected as early as 15 h after axotomy. The elevation of bFGF mRNA and protein levels declined after 1 week. bFGF mRNA was also up-regulated in non-neuronal cells following axotomy. Normally bFGF-LI was mainly localized in the nuclei of DRG neurons and in some nonneuronal cells. After nerve section, bFGF-LI was in addition found in the cytoplasm, and many more bFGF-positive non-neuronal cells were observed. By means of confocal microscopy analysis of axotomized DRGs, some bFGF-LI could be detected in vesicle-like structures in the cytoplasm as well as in the nucleoli, in addition to the nuclear location. Application of leukaemia inhibitory factor to the transected sciatic nerve significantly increased the number of bFGF-positive neurons, whereas the bFGF-LI in non-neuronal cells was strongly suppressed. About 70% of the normal DRG neurons expressed aFGF mRNA and aFGF-LI. Axotomy produced a moderate increase in aFGF mRNA levels, but no detectable effect on protein levels. Taken together, the results show that bFGF may be involved in the neuronal response to injury and suggest a role in neuronal survival and regeneration in axotomized DRG neurons.