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首页> 外文期刊>Journal of Cellular Physiology >Stepwise up-regulation of microRNA expression levels from replicating to reversible and irreversible growth arrest states in WI-38 human fibroblasts.
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Stepwise up-regulation of microRNA expression levels from replicating to reversible and irreversible growth arrest states in WI-38 human fibroblasts.

机译：逐步上调的microRNA的表达从复制到可逆和水平不可逆转的增长在WI-38逮捕州人类成纤维细胞。

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MicroRNAs (miRNAs) are small non-coding RNAs that regulate diverse genetic expression networks through their control of mRNA stability or translation. Their role in aging mechanisms has been proposed in various model systems. In this report, the expression profiling of 462 human miRNAs in the reversible growth arrest state of quiescence, and irreversible states of replicative senescence and hydrogen peroxide-induced premature senescence, are compared to young replicating lung fibroblasts. Greater numbers of up-regulated than down-regulated miRNAs are observed when cells stop proliferating, particularly in premature senescence, somewhat less in replicative senescence, and less still in quiescence. Several altered miRNA expressions are shared by the three growth arrest states, including the up-regulation of miR-34a, -624, -638 and miR-377, and the down-regulation of miR-365 and miR-512-5p. miRNAs up-regulated in both permanent growth arrest states but not in quiescence include let-7g, miR-26a, -136, -144, -195 and miR-200b. In each of the growth arrest states, miR-34a and let-7f have the most robust up-regulation in H(2)O(2)-induced premature senescence, followed by miR-638 and miR-663 in replicative senescence, and finally, miR-331-3p and miR-595 in quiescence. Our comprehensive evaluation of miRNA target correlations with known biomarkers for replicative senescence suggests that miRNAs may repress pathways controlling not only cell cycle traverse and proliferation, but also insulin-like signaling, DNA repair and apoptosis, all of which are cellular functions deficient in senescent human fibroblasts.
机译：小分子核糖核酸(microrna)是小非编码rna调节多种基因表达网络通过他们控制的信使rna或稳定翻译。提出了各种模型系统。462人的报告,表达分析microrna可逆增长逮捕的状态沉默、不可逆的复制衰老和氢peroxide-induced过早衰老,而年轻的复制肺成纤维细胞。更多的差异理气microrna时观察到的细胞停止增殖,尤其是在为时过早在复制衰老,有点少衰老,少还在沉默。改变三个共享microrna的表达增长逮捕,包括上调miR-34a, -624年,-638年和mir - 377,下调mir - 365和mir - 512 - 5 - p。上调永久增长被捕但不包括静止let-7g,miR-26a, -136、-144、-195和mir - 200 - b。增长的逮捕,miR-34a let-7f最健壮的上调吗全身的H (2) O(2)过早衰老,紧随其后mir - 638和mir - 663在复制衰老,最后,mir - 331 - 3 - p和mir - 595静止。目标的相关性与已知的生物标志物复制衰老表明microrna不仅抑制通路控制细胞周期遍历和增殖,而且胰岛素样信号,DNA修复和细胞凋亡衰老的细胞功能缺陷吗人类成纤维细胞。

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