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轴突切断后成年视网膜神经节细胞中的细胞凋亡。

Apoptosis in adult retinal ganglion cells after axotomy.

作者信息

Garcia-Valenzuela E, Gorczyca W, Darzynkiewicz Z, Sharma S C

机构信息

Department of Cell Biology, New York Medical College, Valhalla 10595.

出版信息

J Neurobiol. 1994 Apr;25(4):431-8. doi: 10.1002/neu.480250408.

Abstract

Lesions to the mature mammalian central nervous system cause irreversible degeneration, in which neurons have been previously thought to be passive victims. In this study, axon-lesioned adult rat neurons are shown instead to actively degrade themselves through the process of apoptosis: a programmed type of cell death in which the cellular apparatus is actively involved in the degradation process. To investigate whether retinal ganglion cells of an adult mammal follow an apoptotic type of death when their axons are severed, DNA breaks in nuclei were labeled in situ, using a method that specifically incorporates biotinylated deoxynucleotides by exogenous terminal deoxynucleotidyl transferase on the 3'-OH ends of DNA. The active nature of the death mechanism was demonstrated by the reduction in biotin-labeled nuclei after administering the protein synthesis inhibitor cycloheximide. Our results suggest that retinal ganglion cells of the adult rat die through apoptosis when axotomized. This raises new possibilities in the treatment of CNS injuries, by the potential interruptibility of a program for neuronal death.

摘要

成熟哺乳动物中枢神经系统的损伤会导致不可逆的退化,在此过程中,神经元曾被认为是被动的受害者。而在本研究中,轴突损伤的成年大鼠神经元被证明是通过凋亡过程主动进行自我降解的:凋亡是一种程序性细胞死亡,在此过程中细胞机制积极参与降解过程。为了研究成年哺乳动物的视网膜神经节细胞在轴突被切断时是否遵循凋亡性死亡,利用一种通过外源末端脱氧核苷酸转移酶将生物素化脱氧核苷酸特异性掺入DNA的3'-OH末端的方法,对细胞核中的DNA断裂进行原位标记。通过给予蛋白质合成抑制剂环己酰亚胺后生物素标记细胞核数量的减少,证明了死亡机制的活性本质。我们的结果表明,成年大鼠的视网膜神经节细胞在轴突切断后通过凋亡死亡。这为中枢神经系统损伤的治疗带来了新的可能性,因为神经元死亡程序可能具有可中断性。

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