Gushchina S V, Volkova O V, Krugliakov P P, Magoulas K B
Morfologiia. 2010;137(3):22-6.
Nuclear factor kappaB (NF-kappaB) controls the expression of multiple anti/proapoptotic genes, including those in the nervous cells. Intranuclear deacetylation and acetylation events are implicated in the regulation of NF-kappaB transcriptional activity. The goal of the work was to demonstrate the transcriptional activity of NF-kappaB in the sensory neurons in vitro and to find out whether NF-kappaB activity could be controlled by modification of acetylation processes, using a transgenic line of NF-kappaB reporter mice in which activation of NF-kappaB drives the expression of the lac-z gene. We show that the expression of the reporter gene was absent in transgenic neurons cultured in normal growth medium or stimulated by TNF-alpha. However, NF-kappaB transcriptional activity in most neurons was induced by in vitro exposure to Trichostatin A, which is a specific inhibitor of histone deacetylases. Taken together our results show that the transcriptional activity of NF-kappaB is limited in sensory neurons due to a transcriptional repression mechanism mediated by histone deacetylases.
核因子κB（NF-κB）控制多种抗凋亡/促凋亡基因的表达，包括神经细胞中的那些基因。细胞核内的去乙酰化和乙酰化事件与NF-κB转录活性的调节有关。这项工作的目的是在体外证明感觉神经元中NF-κB的转录活性，并利用NF-κB报告基因小鼠的转基因品系来找出NF-κB活性是否可以通过乙酰化过程的修饰来控制，在该转基因品系中NF-κB的激活驱动lac-z基因的表达。我们发现，在正常生长培养基中培养或用肿瘤坏死因子-α刺激的转基因神经元中，报告基因没有表达。然而，大多数神经元中的NF-κB转录活性是由体外暴露于曲古抑菌素A诱导的，曲古抑菌素A是组蛋白去乙酰化酶的特异性抑制剂。综合我们的结果表明，由于组蛋白去乙酰化酶介导的转录抑制机制，NF-κB的转录活性在感觉神经元中受到限制。
