Up-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR1

Abstract MicroRNAs (miRNAs) are small noncoding RNA molecules that play important roles in various biological processes. Much evidence shows that miRNAs are closely associated with numerous virus infections; however, involvement of cellular miRNAs in influenza A virus (IAV) infection is unclear. Her...

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Autores principales: Sen Zhang, Jing Li, Junfeng Li, Yinhui Yang, Xiaoping Kang, Yuchang Li, Xiaoyan Wu, Qingyu Zhu, Yusen Zhou, Yi Hu
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Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/a944f0ed5d644c42a79792fc2b06c097
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spelling oai:doaj.org-article:a944f0ed5d644c42a79792fc2b06c0972021-12-02T16:08:01ZUp-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR110.1038/s41598-018-25073-92045-2322https://doaj.org/article/a944f0ed5d644c42a79792fc2b06c0972018-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-25073-9https://doaj.org/toc/2045-2322Abstract MicroRNAs (miRNAs) are small noncoding RNA molecules that play important roles in various biological processes. Much evidence shows that miRNAs are closely associated with numerous virus infections; however, involvement of cellular miRNAs in influenza A virus (IAV) infection is unclear. Here, we found that expression of miR-203 was up-regulated markedly via two different mechanisms during IAV infection. First, we examined the effects of type I interferon induced by IAV on direct activation of miR-203 expression. Next, we showed that DNA demethylation within the miR-203 promoter region in A549 cells induced its up-regulation, and that expression of DNA methyltransferase 1 was down-regulated following H5N1 virus infection. Ectopic expression of miR-203 in turn inhibited H5N1 virus replication by targeting down-regulator of transcription 1 (DR1), which was identified as a novel target of miR-203. Silencing DR1 in miR-203 knockout cells using a specific siRNA inhibited replication of the H5N1 virus, an effect similar to that of miR-203. In summary, the data show that host cell expression of miR-203 is up-regulated upon IAV infection, which increases antiviral responses by suppressing a novel target gene, DR1. Thus, we have identified a novel mechanism underlying the relationship between miR-203 and IAV infection.Sen ZhangJing LiJunfeng LiYinhui YangXiaoping KangYuchang LiXiaoyan WuQingyu ZhuYusen ZhouYi HuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-15 (2018)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Sen Zhang
Jing Li
Junfeng Li
Yinhui Yang
Xiaoping Kang
Yuchang Li
Xiaoyan Wu
Qingyu Zhu
Yusen Zhou
Yi Hu
Up-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR1
description Abstract MicroRNAs (miRNAs) are small noncoding RNA molecules that play important roles in various biological processes. Much evidence shows that miRNAs are closely associated with numerous virus infections; however, involvement of cellular miRNAs in influenza A virus (IAV) infection is unclear. Here, we found that expression of miR-203 was up-regulated markedly via two different mechanisms during IAV infection. First, we examined the effects of type I interferon induced by IAV on direct activation of miR-203 expression. Next, we showed that DNA demethylation within the miR-203 promoter region in A549 cells induced its up-regulation, and that expression of DNA methyltransferase 1 was down-regulated following H5N1 virus infection. Ectopic expression of miR-203 in turn inhibited H5N1 virus replication by targeting down-regulator of transcription 1 (DR1), which was identified as a novel target of miR-203. Silencing DR1 in miR-203 knockout cells using a specific siRNA inhibited replication of the H5N1 virus, an effect similar to that of miR-203. In summary, the data show that host cell expression of miR-203 is up-regulated upon IAV infection, which increases antiviral responses by suppressing a novel target gene, DR1. Thus, we have identified a novel mechanism underlying the relationship between miR-203 and IAV infection.
format article
author Sen Zhang
Jing Li
Junfeng Li
Yinhui Yang
Xiaoping Kang
Yuchang Li
Xiaoyan Wu
Qingyu Zhu
Yusen Zhou
Yi Hu
author_facet Sen Zhang
Jing Li
Junfeng Li
Yinhui Yang
Xiaoping Kang
Yuchang Li
Xiaoyan Wu
Qingyu Zhu
Yusen Zhou
Yi Hu
author_sort Sen Zhang
title Up-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR1
title_short Up-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR1
title_full Up-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR1
title_fullStr Up-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR1
title_full_unstemmed Up-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR1
title_sort up-regulation of microrna-203 in influenza a virus infection inhibits viral replication by targeting dr1
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/a944f0ed5d644c42a79792fc2b06c097
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