Mechanical injury increases bFGF and CNTF mRMA expression in the mouse retina
Mechanical injury increases bFGF and CNTF mRMA expression in the mouse retina
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DOI：
10.1006/exer.1997.0328
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发表时间：
1997-08-01
影响因子：
3.4
通讯作者：
Steinberg, RH
中科院分区：
文献类型：
--
作者：
Cao, W;Wen, R;Steinberg, RH
我们通过检测碱性成纤维细胞生长因子（bFGF）、睫状神经营养因子（CNTF）及其受体FGF受体-1（FGFR-1）和CNTF受体α（CNTFR-alpha）的mRNA表达，来表征正常小鼠视网膜对机械损伤的存活因子反应。通过穿过脉络膜和视网膜色素上皮形成切口，穿透成年BALB/c小鼠每只眼睛的视网膜下腔，损伤视网膜。伤后6小时、12小时、1、2、4、7、10和16天取视网膜。对照组动物无损伤。采用北方印迹法检测bFGF、CNTF及其受体mRNA水平。bFGF和CNTF mRNA在损伤后显著增加，沿着胶质细胞酸性蛋白（GFAP）表达增加。伤后6小时bFGF mRNA表达上调2倍以上，伤后2天达最大值，5倍以上，随后缓慢下降，至伤后16天仍为对照组的2.5倍。CNTF的表达在损伤后6小时显示约1.6倍的小幅增加。上调在损伤后第4天达到约2.7倍的峰值水平，然后在第16天下降至对照水平。在损伤后6、12和24小时，FGFR-1仅有非常小的增加，并且在损伤后1天以上的时间点，FGFR-1没有显著增加。GFAP的表达遵循的时间过程类似的bFGF。我们得出结论，机械损伤诱导bFGF，CNTF，和GFAP的表达在小鼠视网膜中的时间过程类似的这些分子在大鼠视网膜的上调。然而，与大鼠视网膜中的上调相比，损伤诱导的bFGF和GFAP的上调在小鼠视网膜中少得多。此外，在小鼠视网膜中仅存在FGFR-1表达的非常小的诱导。这些结局可以至少部分地解释小鼠视网膜中缺乏损伤诱导的光感受器保护。(C)出版社：Academic Press Limited。
We characterized the survival-factor response of the normal mouse retina to mechanical injury by examining the expression of mRNAs for basic fibroblast growth factor (bFGF), ciliary neurotrophic factor (CNTF), and their receptors, FGF receptor-1 (FGFR-1) and CNTF receptor alpha (CNTFR-alpha). The retina was injured by making an incision through the choroid and retinal pigment epithelium that penetrated the subretinal space of each eye of an adult BALB/c mouse. Retinas were taken 6 hr, 12 hr, 1, 2, 4, 7, 10 and 16 days post-injury. Control animals were without injury. Northern blot analysis was performed to determine bFGF, CNTF and their receptor mRNA levels. A significant increase in bFGF and CNTF mRNAs was observed after injury, along with an increase in glial fibrillary acidic protein (GFAP) expression. More than 2-fold of upregulation of bFGF mRNA was seen as early as 6 hr after injury, This increase reached a maximum of more than 5-fold at day 2 post-injury and then declined slowly, and was still about 2.5-fold of the control level by day 16. Expression of CNTF showed a small increase of about 1.6-fold at 6 hr after injury. The upregulation reached a peak level of about 2.7-fold at day 4 after injury, then declined to control level by day 16. There was only a very small increase in FGFR-1 at 6, 12 and 24 hr after injury, and no significant increases in FGFR-1 at time points longer than 1 day post-injury. Expression of GFAP followed a time course similar to that of bFGF.We conclude that mechanical injury induces bFGF, CNTF, and GFAP expression in the mouse retina with time courses similar to the upregulation of these molecules in rat retina. Compared to the upregulation in rat retina, however, the injury-induced upregulation of bFGF and GFAP is much less in the mouse retina. In addition, there was only a very small induction of FGFR-1 expression in the mouse retina, These Endings may explain, at least in part, the lack of injury-induced photoreceptor protection in the mouse retina. (C) 1997 Academic Press Limited.