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首页> 外文期刊>The European Journal of Neuroscience >Regenerative and survival capabilities of Purkinje cells overexpressing c-Jun.
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Regenerative and survival capabilities of Purkinje cells overexpressing c-Jun.

机译：过度表达c-Jun的Purkinje细胞的再生和存活能力。

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摘要

Following axotomy, cerebellar Purkinje cells (PCs) do not elongate their axons, even in a favourable environment, and are resistant to death. They have no constitutive presence of common growth-associated proteins, such as GAP-43 and c-Jun Previous experiments show that injured transgenic PCs overexpressing GAP-43 exhibit a profuse sprouting along the axon and at its severed end. Nevertheless, the lesioned axons are unable to regenerate either spontaneously or into growth-permissive environments. In addition, a considerable number of GAP-43 transgenic PCs degenerate after injury. c-Jun is an inducible transcription factor expressed in axotomized central neurons and regenerating peripheral neurons. It also contributes to programmed cell death during development. To test whether c-Jun could modify the response of PCs to axotomy or enhance the growth/death phenomena of GAP-43 Purkinje neurons, we generated transgenic mice overexpressing c-Jun in PCs. However, c-Jun upregulation did not affect the adult intact phenotype of these neurons and their regenerative and survival capabilities after axotomy. Also in the cross-bred GAP-43/c-Jun mice, c-Jun did not modify the response of GAP-43 PCs to axotomy. By contrast, in organotypic cultures of cerebellum taken from 9-day-old-pups, the survival capabilities of PCs overexpressing c-Jun decreased, in association with a consistent c-Jun phosphorylation. On the whole our data show that c-Jun alone is unable to trigger regenerative or degenerative phenomena in PCs and suggest that the cellular action of this early gene in developing and mature neurons strongly depends on interplaying intracellular signals.
机译：轴切术后，小脑浦肯野细胞（PCs）即使在良好的环境中也不会延长其轴突，并且具有抗死亡的能力。它们没有常见的生长相关蛋白（例如GAP-43和c-Jun）的组成型存在。先前的实验表明，过量表达GAP-43的受伤转基因PC在轴突及其切断末端显示出大量萌芽。然而，病变的轴突不能自发再生或进入允许生长的环境。另外，大量的GAP-43转基因PC在损伤后退化。 c-Jun是在轴突切除的中枢神经元和再生外周神经元中表达的诱导型转录因子。它还有助于发育过程中的程序性细胞死亡。为了测试c-Jun是否可以修改PC对轴切术的反应或增强GAP-43浦肯野神经元的生长/死亡现象，我们生成了在PC中过表达c-Jun的转基因小鼠。但是，c-Jun上调并不影响这些神经元的成人完整表型及其在轴切术后的再生和生存能力。同样在杂交的GAP-43 / c-Jun小鼠中，c-Jun并未改变GAP-43 PC对轴切术的反应。相比之下，在取自9日龄幼崽的小脑的器官型培养物中，过表达c-Jun的PC的生存能力下降，并伴随c-Jun的磷酸化。总体而言，我们的数据表明，仅c-Jun不能触发PC中的再生或变性现象，并表明该早期基因在发育中和成熟神经元中的细胞作用强烈依赖于相互作用的细胞内信号。

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