Complementary deoxyribonucleic acid microarray data from 36 mice subjected for 1, 2, or 4 weeks of their early life to normal atmospheric conditions (normoxia) or chronic intermittent (CIH) or constant (CCH) hypoxia were analyzed to extract organizational principles of the developing heart transcriptome and determine the integrated response to oxygen deprivation. Although both CCH and CIH regulated numerous genes involved in a wide diversity of processes, the changes in maturational profile, expression stability, and coordination were vastly different between the two treatments, indicating the activation of distinct regulatory mechanisms of gene transcription. The analysis focused on the main regulators of translation and response to stress because of their role in the cardiac hypertrophy and cell survival in hypoxia. On average, the expression of each heart gene was tied to the expression of about 20% of other genes in normoxia but to only 8% in CCH and 9% in CIH, indicating a strong decoupling effect of hypoxia. In contrast to the general tendency, the interlinkages among components of the translational machinery and response to stress increased significantly in CIH and much more in CCH, suggesting a coordinated response to the hypoxic stress. Moreover, the transcriptomic networks were profoundly and differently remodeled by CCH and CIH.

中文翻译：

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对心脏慢性缺氧的综合转录组反应：细胞存活中的翻译调节剂和对压力的反应。

分析来自 36 只小鼠在其早期生活中 1、2 或 4 周处于正常大气条件（常氧）或慢性间歇 (CIH) 或持续 (CCH) 缺氧的互补脱氧核糖核酸微阵列数据，以提取发育中心脏的组织原理转录组并确定对缺氧的综合反应。尽管 CCH 和 CIH 都调控了涉及广泛多样性过程的众多基因，但两种处理在成熟谱、表达稳定性和协调方面的变化有很大不同，表明基因转录的不同调控机制被激活。分析重点关注翻译和应激反应的主要调节因子，因为它们在缺氧条件下的心脏肥大和细胞存活中发挥作用。一般，每个心脏基因的表达与正常氧中约 20% 的其他基因的表达相关，但在 CCH 中仅 8% 和 CIH 中仅 9%，表明缺氧的强烈解耦效应。与一般趋势相反，CIH 中翻译机制组件之间的相互联系和对压力的反应显着增加，而在 CCH 中更多，表明对缺氧应激的协调反应。此外，CCH 和 CIH 对转录组网络进行了深刻而不同的改造。在 CIH 和 CCH 中，翻译机制各组成部分之间的相互联系和对压力的反应显着增加，这表明对缺氧应激的协调反应。此外，CCH 和 CIH 对转录组网络进行了深刻而不同的改造。在 CIH 和 CCH 中，翻译机制各组成部分之间的相互联系和对压力的反应显着增加，这表明对缺氧应激的协调反应。此外，CCH 和 CIH 对转录组网络进行了深刻而不同的改造。