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首页> 外文期刊>American Journal of Physiology >Dynamic changes of gene expression in hypoxia-induced right ventricular hypertrophy.
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Dynamic changes of gene expression in hypoxia-induced right ventricular hypertrophy.

机译：缺氧诱导的右室肥厚中基因表达的动态变化。

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Hypobaric hypoxia induces right ventricular hypertrophy. The relative contribution of pulmonary hypertension, decreased arterial oxygen, and neuroendocrine stimulation to the transcriptional profile of hypoxia-induced right ventricular hypertrophy is unknown. Whereas both ventricles are exposed to hypoxia and neuroendocrine stimulation, only the right ventricle is exposed to increased load. We postulated that right ventricular hypertrophy would reactivate the fetal gene transcriptional profile in response to increased load. We measured the expression of candidate genes in the right ventricle of rats exposed to hypobaric hypoxia (11% O(2)) and compared the results with the left ventricle. Hypoxia induced right ventricular hypertrophy without fibrosis. In the right ventricle only, atrial natriuretic factor transcript levels progressively increased starting at day 7. Metabolic genes were differentially regulated, suggesting a substrate switch from fatty acids to glucose during early hypoxia and a switch back to fatty acids by day 14. There was also a switch in myosin isogene expression and a downregulation of sarcoplasmic/endoplasmic ATPase 2a during early hypoxia, whereas later, both myosin isoforms and SERCA2a were upregulated. When the right and left ventricle were compared, the transcript levels of all genes, except for myosin isoforms and pyruvate dehydrogenase kinase-4, differed dramatically suggesting that all these genes are regulated by load. Our findings demonstrate that hypoxia-induced right ventricular hypertrophy transiently reactivates the fetal gene program. Furthermore, myosin iso-gene and pyruvate dehydrogenase kinase-4 expression is not affected by load, suggesting that either hypoxia itself or neuroendocrine stimulation is the primary regulator of these genes.
机译：低压低氧引起右心室肥大。肺动脉高压，动脉血氧减少和神经内分泌刺激对缺氧诱导的右心室肥大的转录特征的相对贡献尚不清楚。尽管两个心室都暴露于缺氧和神经内分泌刺激下，但仅右心室暴露于增加的负荷下。我们推测右心室肥大将响应增加的负荷而重新激活胎儿基因的转录谱。我们测量了暴露于低压缺氧（11％O（2））大鼠右心室中候选基因的表达，并将结果与​​左心室进行了比较。低氧引起的右心室肥大，无纤维化。仅在右心室，心房利钠因子的转录物水平从第7天开始逐渐增加。代谢基因受到差异调节，表明在早期缺氧期间底物从脂肪酸转换为葡萄糖，并在第14天转换为脂肪酸。缺氧早期缺氧时肌球蛋白同基因表达的变化和肌浆/内质ATPase 2a的下调，而后来，肌球蛋白同工型和SERCA2a均被上调。当比较左右心室时，除肌球蛋白同工型和丙酮酸脱氢酶激酶4外，所有基因的转录水平均显着不同，表明所有这些基因均受负荷调节。我们的发现表明，低氧引起的右心室肥大会暂时重新激活胎儿基因程序。此外，肌球蛋白同基因和丙酮酸脱氢酶激酶4的表达不受负荷的影响，表明缺氧本身或神经内分泌刺激是这些基因的主要调节器。

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