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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Short interfering RNA-mediated silencing of glutaredoxin 2 increases the sensitivity of HeLa cells toward doxorubicin and phenylarsine oxide.
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Short interfering RNA-mediated silencing of glutaredoxin 2 increases the sensitivity of HeLa cells toward doxorubicin and phenylarsine oxide.

机译：短干扰RNA介导的谷胱甘肽2沉默可增加HeLa细胞对阿霉素和苯ar氧化物的敏感性。

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摘要

Glutaredoxin (Grx) belongs to the thioredoxin fold superfamily and catalyzes glutathione-dependent oxidoreductions. The recently discovered mitochondrial and nuclear Grx (Grx2) differs from the more abundant cytosolic Grx (Grx1) by its higher affinity toward S-glutathionylated proteins and by being a substrate for thioredoxin reductase. Here, we have successfully established a method to silence the expression of Grx2 in HeLa cells by using short interfering RNA to study its role in the cell. Cells with levels of Grx2 <3% of the control were dramatically sensitized to cell death induced by doxorubicin/adriamycin and phenylarsine oxide but did not show signs of a general increase in oxidative damage with respect to carbonylation and glutathionylation. The ED(50) for doxorubicin dropped from 40 to 0.7 microM and for phenylarsine oxide from 200 to 5 nM. However, no differences were detected after treatment with cadmium, a known inhibitor of Grx1. These results indicate a crucial role of Grx2 in the regulation of the mitochondrial redox status and regulation of cell death at the mitochondrial checkpoint.
机译：谷胱甘肽毒素（Grx）属于硫氧还蛋白折叠超家族，催化谷胱甘肽依赖性氧化还原。最近发现的线粒体和核Grx（Grx2）与更丰富的胞质Grx（Grx1）不同，因为它对S-谷胱甘肽化蛋白的亲和力更高，并且是硫氧还蛋白还原酶的底物。在这里，我们已经成功地建立了一种通过使用短干扰RNA来研究Hex细胞在HeLa细胞中沉默Grx2表达的方法。具有Grx2 <3％对照水平的细胞对由阿霉素/阿霉素和苯ar氧化物诱导的细胞死亡显着敏感，但在羰基化和谷胱甘肽化方面没有显示出氧化损伤的普遍增加的迹象。阿霉素的ED（50）从40降至0.7 microM，苯M氧化物的ED（50）从200降至5 nM。但是，用镉（一种已知的Grx1抑制剂）处理后未发现差异。这些结果表明，Grx2在调节线粒体氧化还原状态和调节线粒体检查点细胞死亡中起着至关重要的作用。

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