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Transcriptional responses of neonatal mouse lung to hyperoxia by Nrf2 status

机译：Nrf2状态对新生小鼠肺对高氧的转录反应

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摘要

Hyperoxia exposure can inhibit alveolar growth in the neonatal lung through induction of p21/p53 pathways and is a risk factor for the development of bronchopulmonary dysplasia (BPD) in preterm infants. We previously found that activation of nuclear factor erythroid 2 p45-related factor (Nrf2) improved survival in neonatal mice exposed to hyperoxia likely due to increased expression of anti-oxidant response genes. It is not known however, whether hyperoxic induced Nrf2 activation attenuates the growth impairment caused by hyperoxia in neonatal lung. To determine if Nrf2 activation modulates cell cycle regulatory pathway genes associated with growth arrest we examined the gene expression in the lungs of Nrf2-/- and Nrf2+/+ neonatal mice at one and 3days of hyperoxia exposure. Methods: Microarray analysis was performed in neonatal Nrf2+/+ and Nrf2-/- lungs exposed to one and 3days of hyperoxia. Sulforaphane, an inducer of Nrf2 was given to timed pregnant mice to determine if in utero exposure attenuated p21 and IL-6 gene expression in wildtype neonatal mice exposed to hyperoxia. Results: Cell cycle regulatory genes were induced in Nrf2-/- lung at 1day of hyperoxia. At 3days of hyperoxia, induction of cell cycle regulatory genes was similar in Nrf2+/+ and Nrf2-/- lungs, despite higher inflammatory gene expression in Nrf2-/- lung. Conclusion: p21/p53 pathways gene expression was not attenuated by Nrf2 activation in neonatal lung. In utero SUL did not attenuate p21 expression in wildtype neonatal lung exposed to hyperoxia. These findings suggest that although Nrf2 activation induces expression of anti-oxidant genes, it does not attenuate alveolar growth arrest caused by exposure to hyperoxia.
机译：高氧暴露可通过诱导p21 / p53途径抑制新生儿肺泡生长，并且是早产儿发生支气管肺发育不良（BPD）的危险因素。我们先前发现，激活核因子红系2 p45相关因子（Nrf2）可以改善暴露于高氧血症的新生小鼠的存活率，这可能是由于抗氧化反应基因表达增加所致。然而，尚不清楚高氧诱导的Nrf2激活是否能减轻新生儿肺中高氧引起的生长障碍。为了确定Nrf2激活是否调节与生长停滞相关的细胞周期调控途径基因，我们检查了高氧暴露1天和3天时Nrf2-/-和Nrf2 + / +新生小鼠肺中的基因表达。方法：对暴露于高氧血症1天和3天的新生儿Nrf2 + / +和Nrf2-/-肺进行芯片分析。向定时怀孕的小鼠给予Nrf2的诱导剂萝卜硫素，以确定是否在子宫内暴露会使暴露于高氧血症的野生型新生小鼠的p21和IL-6基因表达减弱。结果：高氧第1天在Nrf2-/-肺中诱导了细胞周期调控基因。高氧3天后，尽管Nrf2-/-肺中的炎症基因表达较高，但Nrf2 + / +和Nrf2-/-肺中细胞周期调控基因的诱导相似。结论：新生肺中Nrf2的激活不能减弱p21 / p53通路的基因表达。在子宫内，SUL不会减弱暴露于高氧血症的野生型新生儿肺中的p21表达。这些发现表明，尽管Nrf2激活诱导了抗氧化基因的表达，但它并没有减弱由暴露于高氧引起的肺泡生长停滞。

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