Of mice and men: correlations between microRNA-17∼92 cluster expression and promoter methylation in severe bronchopulmonary dysplasia
Of mice and men: correlations between microRNA-17∼92 cluster expression and promoter methylation in severe bronchopulmonary dysplasia
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DOI：
10.1152/ajplung.00390.2016
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发表时间：
2016-11-01
影响因子：
4.9
通讯作者：
Tipple, Trent E.
中科院分区：
文献类型：
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作者：
Robbins, Mary E.;Dakhlallah, Duaa;Tipple, Trent E.
我们先前证明，类似于92簇表达的miR-17减少1）存在于死于支气管肺发育不良（BPD）的人类婴儿的肺部; 2）与DNA甲基转移酶（DNMT）表达和启动子甲基化负相关; 3）与随后在36周胎龄诊断BPD相关。我们检验了这样的假设，即血浆miR-17水平在最终发展为严重BPD的婴儿中最低。其次，我们利用我们充分表征的重度BPD小鼠模型，该模型结合了围产期炎症和出生后高氧，以检验我们模型中肺miR-17类似于92、DNMT和启动子甲基化的改变将反映我们在早产儿组织中的发现的假设。在出生后的前5天从早产儿中获得血浆
We previously demonstrated that decreased miR-17 similar to 92 cluster expression was 1) present in lungs from human infants who died with bronchopulmonary dysplasia (BPD); 2) inversely correlated with DNA methyltransferase (DNMT) expression and promoter methylation; and 3) correlated with a subsequent diagnosis of BPD at 36 wk gestational age. We tested the hypothesis that plasma miR-17 levels would be lowest in infants who ultimately develop severe BPD. Secondly, we utilized our well-characterized murine model of severe BPD that combines perinatal inflammation with postnatal hyperoxia to test the hypothesis that alterations in lung miR-17 similar to 92, DNMT, and promoter methylation in our model would mirror our findings in tissues from premature human infants. Plasma was obtained during the first 5 days of life from premature infants born