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首页> 外文期刊>The Journal of Nutritional Biochemistry >Alteration in methylation pattern of GATA-4 promoter region in vitamin A-deficient offspring's heart.
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Alteration in methylation pattern of GATA-4 promoter region in vitamin A-deficient offspring's heart.

机译：缺乏维生素A的后代心脏中GATA-4启动子区域甲基化模式的变化。

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Epigenetics might explain correlations between lifestyle and risk of disease. Maternal diet has been shown to dynamically alter epigenetic regulation, including affecting DNA methylation status. This study was designed to test the hypothesis that GATA-4 gene methylation would lead to congenital heart defects in vitamin A-deficient offspring. Ten weaning female rats (VAN group) were fed with a diet which contents 4 IU vitamin A/g diet, while 20 rats (VAD group) were maintained on a diet without vitamin A. After 10 weeks of feeding, all the female rats were mated with normal male rats. The VAN group and a portion of VAD group rats were still given the same diet as before mating, while the rest of the rats from the VAD group (VADS group) were transferred to a diet with enough added vitamin A (10 IU/g diet) for the pregnancy cycle. The embryo hearts were dissected out at embryonic day 13.5 (E13.5) for observation of cardiac development, GATA-4 gene methylation status and the expression of DNA methyltransferases (DNMTs). Embryos from vitamin A-deficient group exhibited a high incidence of cardiac defects. High methylation was present in the CpG loci of GATA-4 gene with a low expression of GATA-4 mRNA from vitamin A-deficient group embryos. Moreover, up-regulation of DNMT1 and down-regulation of DNMT3a and DNMT3b expression were found in this group embryo. These findings show that aberrant methylation is one of key mechanisms to heart defects in vitamin A-deficient offspring. DNMTs play a critical role in this process
机译：表观遗传学可以解释生活方式与疾病风险之间的相关性。孕妇饮食已被证明可以动态改变表观遗传调控，包括影响DNA甲基化状态。这项研究旨在检验以下假设：GATA-4基因甲基化会导致维生素A缺乏症后代的先天性心脏缺陷。给十只断奶雌性大鼠（VAN组）喂食含4 IU维生素A / g饮食的饮食，而让二十只大鼠（VAD组）维持不含维生素A的饮食。喂食10周后，所有雌性大鼠与正常的雄性大鼠交配。 VAN组和部分VAD组大鼠仍保持与交配前相同的饮食，而其余的VAD组（VADS组）大鼠转入添加了足够维生素A（10 IU / g饮食）的饮食）的怀孕周期。在胚胎第13.5天（E13.5）解剖胚胎心脏，以观察心脏发育，GATA-4基因甲基化状态和DNA甲基转移酶（DNMT）的表达。维生素A缺乏症组的胚胎表现出较高的心脏缺陷发生率。 GATA-4基因的CpG位点中存在高甲基化，而维生素A缺陷型胚胎中GATA-4 mRNA的表达低。此外，在该组胚胎中发现了DNMT1的上调和DNMT3a和DNMT3b表达的下调。这些发现表明，甲基化异常是缺乏维生素A的后代心脏缺陷的关键机制之一。 DNMT在此过程中起关键作用

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