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首页> 外文期刊>Cell Research >Hypoxia upregulates hypoxia inducible factor (HIF)-3alpha expression in lung epithelial cells: characterization and comparison with HIF-1alpha.
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Hypoxia upregulates hypoxia inducible factor (HIF)-3alpha expression in lung epithelial cells: characterization and comparison with HIF-1alpha.

机译：缺氧上调肺上皮细胞中的缺氧诱导因子（HIF）-3alpha表达：表征和与HIF-1alpha的比较。

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The role of the hypoxia-inducible factor (HIF) subunits 1alpha and 2alpha in response to hypoxia is well established in lung epithelial cells, whereas little is known about HIF-3alpha with respect to transcriptional and translational regulation by hypoxia. HIF-3alpha and HIF-1alpha are two similar but distinct basic helix-loop-helix-PAS proteins, which have been postulated to activate hypoxia responsive genes in response to hypoxia. Here, we used quantitative real time RT-PCR and immunoblotting to determine the activation of HIF-3alpha vs. HIF-1alpha by hypoxia. HIF-3alpha was strongly induced by hypoxia (1% O(2)) both at the level of protein and mRNA due to an increase in protein stability and transcriptional activation, whereas HIF-1alpha protein and mRNA levels enhanced transiently and then decreased because of a reduction in its mRNA stability in A549 cells, as measured on mRNA and protein levels. Interestingly, HIF-3alpha and HIF-1alpha exhibited strikingly similar responses to a variety of activating or inhibitory pharmacological agents. These results demonstrate that HIF-3alpha is expressed abundantly in lung epithelial cells, and that the transcriptional induction of HIF-3alpha plays an important role in the response to hypoxia in vitro. Our findings suggest that HIF-3alpha, as a member of the HIF system, is complementary rather than redundant to HIF-1alpha induction in protection against hypoxic damage in alveolar epithelial cells.Cell Research (2006) 16: 548-558. doi:10.1038/sj.cr.7310072; published online 15 June 2006.
机译：缺氧诱导因子（HIF）亚基1alpha和2alpha响应缺氧的作用在肺上皮细胞中已经确立，而关于HIF-3alpha在缺氧的转录和翻译调控方面知之甚少。 HIF-3alpha和HIF-1alpha是两种相似但截然不同的基本螺旋-环-螺旋-PAS蛋白，据推测它们可以激活对缺氧的缺氧反应基因。在这里，我们使用定量实时RT-PCR和免疫印迹来确定缺氧激活HIF-3alpha与HIF-1alpha。 HIF-3alpha被缺氧（1％O（2））在蛋白质和mRNA水平上强烈诱导，这是由于蛋白质稳定性和转录激活的增加所致，而HIF-1alpha蛋白质和mRNA水平则瞬时升高，然后下降，原因是以mRNA和蛋白质水平衡量，其在A549细胞中的mRNA稳定性降低。有趣的是，HIF-3alpha和HIF-1alpha对多种激活或抑制药理剂表现出惊人的相似反应。这些结果表明，HIF-3alpha在肺上皮细胞中大量表达，并且HIF-3alpha的转录诱导在体外对缺氧的应答中起重要作用。我们的发现表明，作为HIF系统成员的HIF-3α在防止肺泡上皮细胞的低氧损伤方面与HIF-1α诱导互补而不是多余。CellResearch（2006）16：548-558。 doi：10.1038 / sj.cr.7310072; 2006年6月15日在线发布。

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