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碱性成纤维细胞生长因子:在遗传性和光诱导性光感受器变性中基因表达增加。

Basic fibroblast growth factor: increased gene expression in inherited and light-induced photoreceptor degeneration.

作者信息

Gao H, Hollyfield J G

机构信息

Division of Ophthalmology, Research Institute FFb, Cleveland, OH 44195, USA.

出版信息

Exp Eye Res. 1996 Feb;62(2):181-9. doi: 10.1006/exer.1996.0022.

Abstract

In a recent study, we reported that bFGF content and mRNA expression levels are elevated in degenerating photoreceptors in the rd mouse retina as compared to the levels in photoreceptors in age matched normal retinas (Gao and Hollyfield, 1995). To determine whether bFGF up-regulation is a general feature of degenerating photoreceptors, bFGF expression was examined with in situ hybridization in several rodent models with retinal degeneration: (a) the normal mouse retina in which cGMP metabolism had been disrupted pharmacologically using an inhibitor of phosphodiesterase or an analog of cGMP, (b) the rds mouse with an inherited photoreceptor degeneration that does not involve alterations in cGMP metabolism, (c) light-damaged BALB/c mice subjected to bright constant light, and (d) light-stressed albino rats subjected to bright cyclic light. In each of these models, we observed dramatic up-regulation of bFGF gene expression in photoreceptors, although the relative levels varied among the different models and followed different temporal patterns. We conclude that increased expression of bFGF in photoreceptors during their degeneration is a general phenomenon occurring in rd, rds, light-damaging and light-stressing conditions. These observations indicate that bFGF can be up-regulated by a variety of photoreceptor insults. We speculate that endogenous bFGF may function as a photoreceptor protection/rescue factor that is activated in response to photoreceptor stress.

摘要

在最近的一项研究中,我们报告称,与年龄匹配的正常视网膜中的光感受器相比,rd小鼠视网膜中退化的光感受器中的碱性成纤维细胞生长因子(bFGF)含量和mRNA表达水平有所升高(高和霍利菲尔德,1995年)。为了确定bFGF上调是否是退化的光感受器的一个普遍特征,我们在几种视网膜退化的啮齿动物模型中用原位杂交法检测了bFGF的表达:(a)正常小鼠视网膜,其中使用磷酸二酯酶抑制剂或cGMP类似物通过药理学方法破坏了cGMP代谢;(b)rds小鼠,其患有遗传性光感受器退化,不涉及cGMP代谢的改变;(c)暴露于持续强光下的光损伤BALB/c小鼠;(d)暴露于周期性强光下的光应激白化大鼠。在这些模型中的每一个中,我们都观察到光感受器中bFGF基因表达的显著上调,尽管不同模型中的相对水平有所不同,且遵循不同的时间模式。我们得出结论,光感受器在退化过程中bFGF表达增加是一种在rd、rds、光损伤和光应激条件下普遍发生的现象。这些观察结果表明,bFGF可被多种光感受器损伤上调。我们推测内源性bFGF可能作为一种光感受器保护/拯救因子,在光感受器应激时被激活。

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