Expression of c-jun protein in degenerating retinal ganglion cells after optic nerve lesion in the rat
Expression of c-jun protein in degenerating retinal ganglion cells after optic nerve lesion in the rat
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DOI：
10.1006/exnr.1997.6585
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发表时间：
1997-09-01
影响因子：
5.3
通讯作者：
Bahr, M
中科院分区：
文献类型：
--
作者：
Isenmann, S;Bahr, M
视神经轴突损伤诱导大鼠视网膜神经节细胞(RGCs)表达c-jun。使用逆行示踪剂进行的详细研究，以及对c-jun和再生相关因子(如生长相关蛋白GAP-43)的双重标记研究表明，c-jun的上调是受影响的视网膜节细胞存活和再生轴突的流产尝试中细胞体反应的一部分。另一方面，c-jun蛋白在几种神经退行性变中的长时间表达与诱导细胞凋亡有关。本研究采用免疫细胞化学方法检测视神经夹伤后视网膜切片中c-jun蛋白表达的时程和亚细胞定位，并对c-jun蛋白和DNA链断裂进行双标记法检测视网膜组织中的细胞凋亡。损伤后数天可见视网膜神经节细胞亚群，其中c-jun蛋白不仅定位于胞核，而且定位于胞浆。RGCs同时出现凋亡、DNA链断裂和c-jun免疫反应的形态特征。因此，c-jun的表达不仅限于完整或再生的神经节细胞，也存在于注定要死亡的细胞中。我们的结果表明，决定经历任何一种命运取决于额外的信号事件，这些事件调节c-jun的转录行为。(C)1997年学术出版社。
Axonal lesions to the optic nerve (ON) induce c-Jun expression in retinal ganglion cells (RGCs) of the rat in vivo. Detailed investigations using retrograde tracers, and double labeling studies for c-Jun and regeneration-associated factors, such as the growth-associated protein GAP-43, have suggested that this upregulation of c-Jun is part of a cell body response in an abortive attempt of affected RGCs to survive and regenerate an axon. On the other hand, prolonged expression of c-Jun protein has in several paradigms of neurodegeneration been linked to the induction of apoptotic cell death. In the present study, we examined the time course and subcellular localization of c-Jun protein by immunocytochemistry on retinal sections after optic nerve crush and carried out double labeling for c-Jun protein and DNA strand breaks to detect apoptosis on the same sections. Several days after ON lesion, a subpopulation of RGCs was detected in which c-Jun protein was not confined to the nucleus, but also located in the cytoplasm. In addition, RGCs were seen that displayed morphological signs of apoptosis, DNA strand breaks, and c-Jun immunoreactivity at the same time. Therefore, c-Jun expression is not confined to intact or regenerating ganglion cells, but also occurs in cells that are destined to die. Our results suggest that the decision to undergo either fate depends on additional signaling events that modulate the transcriptional actions of c-Jun. (C) 1997 Academic Press.