Pennypacker K
Department of Pharmacology and Therapeutics, University of South Florida, Tampa 33612, USA.
Histol Histopathol. 1997 Oct;12(4):1125-33.
After brain injury, neuronal genes are regulated to adjust to an altered environment; however, if neurons are damaged then genes related apoptosis are activated. Glial cells, astrocytes and microglia, respond to neuronal death by transcribing genes to enhance the survival of remaining neurons and for regeneration and repair. AP-1 transcription factors are induced in the neuronal response to injury. Depending on the AP-1 dimer combination, neuronal genes related to either apoptosis or survival are transcribed. A 35 kDa Fos-related antigen:JunD dimer is present in neurons that survive injury. Jun and JunD exists in neurons prior to undergoing apoptosis. Neuronal death activates gene expression in astrocytes and microglia. NFk beta transcription factors are induced in astrocytes reacting to neuronal injury. In the microglial response, STATs appear to be activated to regulate gene transcription. These transcription factors that modulate the genes involved in the cellular processes of brain injury are examined in this review.
脑损伤后，神经元基因会被调节以适应改变的环境；然而，如果神经元受损，那么与细胞凋亡相关的基因就会被激活。神经胶质细胞、星形胶质细胞和小胶质细胞通过转录基因来响应神经元死亡，以提高剩余神经元的存活率并促进再生和修复。AP-1转录因子在神经元对损伤的反应中被诱导产生。根据AP-1二聚体的组合情况，与细胞凋亡或存活相关的神经元基因会被转录。一种35 kDa的Fos相关抗原：JunD二聚体存在于损伤后存活的神经元中。Jun和JunD在神经元发生凋亡之前就已存在。神经元死亡会激活星形胶质细胞和小胶质细胞中的基因表达。NFkβ转录因子在星形胶质细胞对神经元损伤的反应中被诱导产生。在小胶质细胞的反应中，信号转导和转录激活因子（STATs）似乎被激活以调节基因转录。本综述对这些调节脑损伤细胞过程中相关基因的转录因子进行了研究。
