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首页> 外文期刊>Journal of Cellular Physiology >Hypoxia-induced upregulation of eNOS gene expression is redox-sensitive: a comparison between hypoxia and inhibitors of cell metabolism.
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Hypoxia-induced upregulation of eNOS gene expression is redox-sensitive: a comparison between hypoxia and inhibitors of cell metabolism.

机译：低氧诱导upregulation以挪士的基因表达式是redox-sensitive:比较缺氧和抑制剂的细胞之间新陈代谢。

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Several papers report a hypoxia-induced upregulation of the endothelial nitric oxide synthase (eNOS) mRNA expression. Since there is no known hypoxia-sensitive element binding site in the eNOS promoter, we reasoned that the effect of hypoxia could be simulated by a metabolically elicited alteration of the redox state. Therefore, cultured porcine aortic endothelial cells (PAEC) were exposed to hypoxia (1-10% O(2)) or inhibitors of cellular energy metabolism including rotenone, 2, 4 dinitrophenol (DNP) and 2-deoxyglucose for 6 to 24 h. Additionally, cells were treated with lactate and nicotinic acid to alter the cellular NAD(P)H/NAD(P) ratio without changes of energy supply. The cellular NAD(P)H/NAD(P) ratio was used as an index of the cellular redox state and determined using the MTT-assay. Hypoxia increased eNOS mRNA transcription and MTT-reduction in a manner inversely proportional to pO(2). Exposure to rotenone, DNP, and lactate increased the NAD(P)H/NAD(P) ratio, MTT-reduction, and eNOS mRNA also in parallel. In contrast, 2-deoxyglucose and nicotinic acid attenuated both MTT-reduction and eNOS mRNA expression. In order to study a potential role of the redox regulated transcription factor complex AP-1 in hypoxia-induced eNOS mRNA transcription, c-jun expression was determined and decoy experiments were performed. c-jun expression paralleled changes of eNOS mRNA expression and MTT-reduction. Furthermore, in the presence of oligodeoxynucleotides corresponding to the AP-1 binding sites of the eNOS promoter, the hypoxia and chemically induced eNOS mRNA expression was completely abolished. We propose that hypoxia, by altering cellular metabolism, leads to an increase in the cellular NAD(P)H/NAD(P) ratio which favors enhanced eNOS expression by redox-sensitive AP-1 mediated transcriptional control. Copyright 2001 Wiley-Liss, Inc.
机译：一个低氧诱导的数篇论文报告upregulation内皮一氧化氮合酶(以挪士)mRNA的表达。没有已知hypoxia-sensitive元素结合位点以挪士启动子,我们推断的效果缺氧可能是模拟的新陈代谢引起氧化还原状态的改变。因此,培养猪主动脉内皮细胞(PAEC)暴露在缺氧O (2) (1 - 10%)或细胞能量代谢抑制剂包括鱼藤酮、2,4二硝基酚(DNP)和2-deoxyglucose 6到24 h。此外,细胞乳酸和烟酸治疗改变细胞NAD (P) H / NAD (P)比率能源供应的变化。NAD (P) H / NAD (P)比作为一个索引的细胞氧化还原状态和使用决定MTT-assay。转录和MTT-reduction的方式阿宝(2)成反比。鱼藤酮、DNP和乳酸增加了NAD (P) H / NAD (P)比MTT-reduction,以挪士信使rna也并行。2-deoxyglucose和烟酸减毒MTT-reduction和以挪士mRNA的表达。研究氧化还原调控的潜在作用转录因子复杂AP-1低氧诱导以挪士mRNA转录,c-jun表达决心和诱饵实验被执行。以挪士mRNA的表达和变化MTT-reduction。oligodeoxynucleotides AP-1对应以挪士启动子的结合位点,缺氧和化学诱导以挪士mRNA表达完全废除。改变细胞的代谢,导致一个增加细胞NAD (P) H / NAD (P)的比例这有利于增强以挪士表达redox-sensitive AP-1介导的转录控制。

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