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首页> 外文期刊>Life sciences >Temporal transcriptomic profiling reveals cellular targets that govern survival in HOCl-mediated neuronal apoptosis.
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Temporal transcriptomic profiling reveals cellular targets that govern survival in HOCl-mediated neuronal apoptosis.

机译：时间转录组谱分析揭示了控制HOC1介导的神经元凋亡中生存的细胞靶标。

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AIMS: With the identification of hypochlorous acid (HOCl) as a biomarker in diseased brains and endogenous detection of its modified proteins, HOCl might be implicated in the development of neurodegenerative disorders. However, its effect on neuronal cell death has not yet been investigated at gene expression level. MAIN METHODS: Therefore, DNA microarray was performed for screening of HOCl-responsive genes in primary mouse cortical neurons. Neurotoxicity caused by physiological relevant HOCl (250muM) exhibited several biochemical markers of apoptosis. KEY FINDINGS: The biological processes affected during HOCl-mediated apoptosis included cell death, response to stress, cellular metabolism, and cell cycle. Among them, mRNAs level of cell death and stress response genes were up-regulated while expression of metabolism and cell cycle genes were down-regulated. SIGNIFICANCE: Our results showed, for the first time, that HOCl induces apoptosis in cortical neurons by upregulating apoptotic genes and gene expression of stress response such as heat shock proteins and antioxidant proteins were enhanced to provide protection. These data form a foundation for the development of screening platforms and define targets for intervention in HOCl neuropathologies where HOCl-mediated injury is causative.
机译：目的：随着次氯酸（HOCl）在患病大脑中的生物标记物的鉴定以及其修饰蛋白的内源性检测，HOCl可能与神经退行性疾病的发展有关。但是，尚未在基因表达水平研究其对神经元细胞死亡的影响。主要方法：因此，进行了DNA微阵列筛选，以筛选原代小鼠皮层神经元中的HOCl反应基因。生理相关的HOCl（250μM）引起的神经毒性表现出一些凋亡的生化标记。主要发现：在HOC1介导的细胞凋亡过程中受到影响的生物学过程包括细胞死亡，对压力的反应，细胞代谢和细胞周期。其中，细胞死亡和应激反应基因的mRNA水平上调，而代谢和细胞周期基因的表达下调。意义：我们的结果首次表明，HOCl通过上调凋亡基因来诱导皮层神经元凋亡，并增强了应激反应的基因表达，例如热休克蛋白和抗氧化剂蛋白，从而提供保护作用。这些数据为开发筛选平台奠定了基础，并确定了在HOCl介导的损伤起因的HOCl神经病理学中进行干预的目标。

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