MicroRNA Profiling of Sendai Virus-Infected A549 Cells Identifies miR-203 as an Interferon-Inducible Regulator of IFIT1/ISG56
MicroRNA Profiling of Sendai Virus-Infected A549 Cells Identifies miR-203 as an Interferon-Inducible Regulator of IFIT1/ISG56
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DOI：
10.1128/jvi.01064-13
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发表时间：
2013-08-01
影响因子：
5.4
通讯作者：
Horvath, Curt M.
中科院分区：
文献类型：
--
作者：
Buggele, William A.;Horvath, Curt M.
哺乳动物I型干扰素（IFN）应答是病毒感染的主要屏障，并且对于完全的先天性和适应性免疫是必需的。IFN产生和IFN介导的抗病毒信号传导都是差异细胞基因表达的结果，这是一个在转录和翻译水平上受到严格控制的过程。为了确定微小RNA（miRNA）介导的抗病毒应答调节的潜力，使用小RNA谱分析在稳态和用仙台病毒的Cantell株感染后人A549细胞的miRNA含量，仙台病毒是IFN和细胞抗病毒应答的有效诱导剂。虽然细胞的miRNA含量在很大程度上不受感染的影响，但在仙台病毒感染期间，发现了miRNA丰度的特定变化。发现一种miRNA，miR-203，在感染的细胞中积累并响应IFN治疗。结果表明，miR-203是一种IFN诱导的miRNA，可以通过使其mRNA转录物不稳定来负调节许多细胞mRNA，包括IFN刺激的基因靶点IFIT 1/ISG 56。
The mammalian type I interferon (IFN) response is a primary barrier for virus infection and is essential for complete innate and adaptive immunity. Both IFN production and IFN-mediated antiviral signaling are the result of differential cellular gene expression, a process that is tightly controlled at transcriptional and translational levels. To determine the potential for microRNA (miRNA)-mediated regulation of the antiviral response, small-RNA profiling was used to analyze the miRNA content of human A549 cells at steady state and following infection with the Cantell strain of Sendai virus, a potent inducer of IFN and cellular antiviral responses. While the miRNA content of the cells was largely unaltered by infection, specific changes in miRNA abundance were identified during Sendai virus infection. One miRNA, miR-203, was found to accumulate in infected cells and in response to IFN treatment. Results indicate that miR-203 is an IFN-inducible miRNA that can negatively regulate a number of cellular mRNAs, including an IFN-stimulated gene target, IFIT1/ISG56, by destabilizing its mRNA transcript.