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首页> 外文期刊>Life sciences >Comparison of global DNA methylation profiles in replicative versus premature senescence.
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Comparison of global DNA methylation profiles in replicative versus premature senescence.

机译：比较复制性和过早衰老中的整体DNA甲基化谱。

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DNA methylation is considered to play an essential role in cellular senescence. To uncover the mechanism underlying cellular senescence, we established the model of premature senescence induced by hydrogen peroxide (H(2)O(2)) in human embryonic lung fibroblasts and investigated the changes of genome methylation, DNA methyltransferases (DNMTs) and DNA-binding domain proteins (MBDs) in comparison with those observed during normal replicative senescence. We found that premature senescence triggered by H(2)O(2) exhibited distinct morphological characteristics and proliferative capacity which were similar to those of replicative senescence. The genome methylation level decreased gradually during the premature as well as replicative senescence, which was associated with the reduction in the expression of DNMT1, reflecting global hypomethylation as a distinct feature of senescent cells. The levels of DNMT3b and methyl-CpG binding protein 2 (MeCP2) increased in both mid-aged and replicative senescent cells, while DNMT3a and MBD2 were upregulated in the mid-aged cells. Only DNMT3b was elevated in the cells in the premature senescence persistence status. Additionally, the expression for DNMTs, MBD2 and MeCP2 was increased rapidly upon H(2)O(2) treatment. These results indicate that H(2)O(2)-induced premature senescence share some features of replicative senescence, such as basic biological characteristics and global hypomethylation while there are slight differences in the profile of methylation-associated enzyme expression. Oxidative damage may hence be a causative factor in epigenetic alteration partly responsible for cellular senescence.
机译：DNA甲基化被认为在细胞衰老中起重要作用。为了揭示细胞衰老的机制，我们建立了人类胚胎肺成纤维细胞中过氧化氢（H（2）O（2））诱导的过早衰老模型，并研究了基因组甲基化，DNA甲基转移酶（DNMT）和DNA-结合域蛋白（MBDs）与正常复制衰老过程中观察到的蛋白相比。我们发现由H（2）O（2）触发的过早衰老表现出独特的形态特征和增殖能力，与复制衰老相似。在早衰期和复制性衰老过程中，基因组甲基化水平逐渐降低，这与DNMT1的表达下降有关，反映出总体的低甲基化是衰老细胞的独特特征。 DNMT3b和甲基CpG结合蛋白2（MeCP2）的水平在中年和复制性衰老细胞中均增加，而DNMT3a和MBD2在中年细胞中上调。在早衰持续状态中，仅DNMT3b在细胞中升高。此外，DNMTs，MBD2和MeCP2的表达在H（2）O（2）处理后迅速增加。这些结果表明，H（2）O（2）引起的过早衰老具有复制衰老的一些特征，例如基本生物学特征和全局低甲基化，而甲基化相关酶表达的特征略有差异。因此，氧化损伤可能是表观遗传改变的致病因素，部分原因是细胞衰老。

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