Suppr超能文献

肝脏中毒性损伤后的基因表达:热休克反应及氧化应激诱导基因分析

Gene expression in liver after toxic injury: analysis of heat shock response and oxidative stress-inducible genes.

作者信息

Schiaffonati L, Tiberio L

机构信息

Dipartimento di Scienze Biomediche e Biotecnologie, Università degli Studi di Brescia, Italy.

出版信息

Liver. 1997 Aug;17(4):183-91. doi: 10.1111/j.1600-0676.1997.tb00804.x.

Abstract

In the liver, CCl4 induces cell necrosis followed by regeneration. Cell injury is caused by free radical damage and may be due, at least in part, to oxidative stress and the subsequent formation of reactive oxygen intermediates (ROIs). In a rat model of acute CCl4-induced hepatic injury, we examined the expression of genes involved in cellular response to different kinds of stress, including oxidative stress (hsp 70 family, heme oxygenase), in free radical detoxification (Mn superoxide dismutase and Cu/ Zn superoxide dismutase), in iron homeostasis (H and L ferritin subunits) and in the cell cycle (c-fos, c-jun, histone H3). As an experimental approach, we first analysed the pattern of protein synthesised by liver slices in vitro. Then we studied the mechanisms regulating the expression of different genes, by analysing both mRNA steady state levels and transcription rates. Activation of the specific heat shock transcription factor (HSF) by CCl4 was also investigated. We observed that different members of the hsp70 family (hsp70, hsc73, grp78) are activated by different kinetics and are regulated mainly at the transcriptional level. Induction of the hsp70 gene occurs rapidly and transiently and is preceded by the activation of HSF DNA-binding activity. We demonstrated an increase in the steady-state levels of mRNAs for heme oxygenase, Mn and Cu/Zn superoxide dismutases and H and L ferritin subunits. However, different kinetics and regulatory mechanisms occurred with different genes. We showed that induction of c-fos and c-jun protooncogenes is the earliest event after CCl4 administration, whereas histone H3 expression peaked at 24-48 h. The results of this study are interpreted as evidence that activation of specific stress response genes is primarily related to the defence against the rapidly occurring cell damage, but may also be related to subsequent processes of tissue inflammation and cell proliferation.

摘要

在肝脏中,四氯化碳会引发细胞坏死,随后是再生过程。细胞损伤是由自由基损伤导致的,并且至少部分归因于氧化应激以及随后活性氧中间体(ROIs)的形成。在急性四氯化碳诱导的肝损伤大鼠模型中,我们检测了参与细胞对不同类型应激反应的基因表达,包括氧化应激(热休克蛋白70家族、血红素加氧酶)、自由基解毒(锰超氧化物歧化酶和铜/锌超氧化物歧化酶)、铁稳态(H和L铁蛋白亚基)以及细胞周期(c-fos、c-jun、组蛋白H3)相关基因。作为一种实验方法,我们首先分析了体外肝切片合成蛋白质的模式。然后,通过分析mRNA稳态水平和转录速率,我们研究了调节不同基因表达的机制。我们还研究了四氯化碳对特异性热休克转录因子(HSF)的激活作用。我们观察到热休克蛋白70家族的不同成员(hsp70、hsc73、grp78)以不同的动力学被激活,并且主要在转录水平受到调控。hsp70基因的诱导迅速且短暂,并且在HSF DNA结合活性激活之前发生。我们证明了血红素加氧酶、锰和铜/锌超氧化物歧化酶以及H和L铁蛋白亚基的mRNA稳态水平有所增加。然而,不同基因呈现出不同的动力学和调控机制。我们发现,c-fos和c-jun原癌基因的诱导是四氯化碳给药后最早发生的事件,而组蛋白H3的表达在24 - 48小时达到峰值。本研究结果被解释为证据,表明特异性应激反应基因的激活主要与抵御快速发生的细胞损伤有关,但也可能与随后的组织炎症和细胞增殖过程有关。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验