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首页> 外文期刊>American Journal of Physiology >Regulation of Na-K-ATPase gene expression by hyperoxia in MDCK cells.
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Regulation of Na-K-ATPase gene expression by hyperoxia in MDCK cells.

机译：高氧对MDCK细胞中Na-K-ATPase基因表达的调节。

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摘要

Na-K-ATPase plays a central role in a variety of physiological processes, including ion transport and regulation of cell volume. Our previous data showed that hyperoxia increased the expression of Na-K-ATPase alpha 1 and beta 1 mRNA in lung type II cells. We similarly show that hyperoxia (> or = 95% O2 for 24-48 h) increased steady-state mRNA levels in both Na-K-ATPase subunits in Madin-Darby canine kidney (MDCK) cells. The mechanism of gene regulation by hyperoxia was assessed. Stability of the Na-K-ATPase mRNA levels of both subunits was unchanged in hyperoxia-exposed MDCK cells. To determine whether gene transcription was augmented by hyperoxia, MDCK cells were transfected with a beta 1-subunit promoter-reporter construct. Transfection with the wild-type promoter (beta 1-817) revealed a 1.9 +/- 0.2-fold increase in promoter activity. Transfection with 5' deletion constructs identified a 61-base pair (bp) region between -102 and -41 that was necessary for this increase in promoter activity by hyperoxia. Incorporation of this 61-bp region into a minimal promoter (mouse mammary tumor virus) similarly increased promoter activity 2.3-fold in the presence of hyperoxia. This increase in promoter activity was not seen when MDCK cells were incubated with various concentrations of hydrogen peroxide. In summary, hyperoxia increased Na-K-ATPase beta 1-subunit mRNA steady-state level due to increased transcription in MDCK cells. A region necessary for this hyperoxic effect on beta 1 transcription is located between base pairs -102 and -41 on the promoter.
机译：Na-K-ATPase在各种生理过程中起着核心作用，包括离子转运和细胞体积调节。我们以前的数据表明，高氧会增加II型肺细胞中Na-K-ATPase alpha 1和beta 1 mRNA的表达。我们类似地显示，高氧（>或= 95％O2持续24-48小时）增加了Madin-Darby犬肾（MDCK）细胞中两个Na-K-ATPase亚基的稳态mRNA水平。评估了高氧基因调控的机制。高氧暴露的MDCK细胞中两个亚基的Na-K-ATPase mRNA水平的稳定性均未改变。为了确定高氧血症是否增强了基因转录，将MDCK细胞用β1亚基启动子-报告子构建体转染。用野生型启动子（β1-817）转染显示启动子活性增加1.9 +/- 0.2倍。用5'缺失构建体转染鉴定了-102和-41之间的61个碱基对（bp）区域，这是高氧引起的启动子活性增加所必需的。在高氧存在下，将该61bp的区域掺入最小启动子（小鼠乳腺肿瘤病毒）中，启动子活性类似地增加了2.3倍。当将MDCK细胞与各种浓度的过氧化氢孵育时，看不到启动子活性的增加。总之，由于MDCK细胞中转录的增加，高氧增加了Na-K-ATPaseβ1亚基mRNA稳态水平。这种对beta 1转录的高氧作用所必需的区域位于启动子上的碱基对-102和-41之间。

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