MiR-140 inhibits classical swine fever virus replication by targeting Rab25 in swine umbilical vein endothelial cells

Classical swine fever virus (CSFV) is one of the most important viral pathogens leading worldwide threats to pig industry. MicroRNAs (miRNAs) play important roles in regulating virus replication, but whether miRNAs affect CSFV infection is still poorly understood. In previous study, we identified fo...

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Autores principales: Panpan Xu, Shuangkai Jia, Kai Wang, Zhixin Fan, Hongqing Zheng, Jiangman Lv, Yanfen Jiang, Yufeng Hou, Bihao Lou, Hongchao Zhou, Yanming Zhang, Kangkang Guo
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Publicado: Taylor & Francis Group 2020
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Acceso en línea:https://doaj.org/article/ef501e4aca8841e1b79849b1c6b07bc3
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spelling oai:doaj.org-article:ef501e4aca8841e1b79849b1c6b07bc32021-11-17T14:21:58ZMiR-140 inhibits classical swine fever virus replication by targeting Rab25 in swine umbilical vein endothelial cells2150-55942150-560810.1080/21505594.2020.1735051https://doaj.org/article/ef501e4aca8841e1b79849b1c6b07bc32020-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21505594.2020.1735051https://doaj.org/toc/2150-5594https://doaj.org/toc/2150-5608Classical swine fever virus (CSFV) is one of the most important viral pathogens leading worldwide threats to pig industry. MicroRNAs (miRNAs) play important roles in regulating virus replication, but whether miRNAs affect CSFV infection is still poorly understood. In previous study, we identified four miRNAs that were down-regulated by CSFV in swine umbilical vein endothelial cells (SUVEC). In this study, miR-140, one of the most potently down-regulated genes was investigated. We found that the miRNA expression was significantly inhibited by CSFV infection. Subsequent studies revealed that miR-140 mimics significantly inhibited CSFV replication, while the inhibition of endogenous miR-140 enhanced CSFV replication. By using bioinformatics prediction, luciferase reporter system, real-time fluorescence quantitative PCR (RT-qPCR) and Western blot assays, we further demonstrated that miR-140 bind to the 3ʹ UTR of Rab25 mRNA to regulate its expression. We also analyzed the expression pattern of Rab25 in SUVECs after CSFV infection. The results showed that CSFV infection induced Rab25 expression. Finally, Rab25 was found to promote CSFV replication. In conclusion, this study demonstrated that CSFV inhibits miR-140 expression and miR-140 inhibits replication by binding to host factor Rab25.Panpan XuShuangkai JiaKai WangZhixin FanHongqing ZhengJiangman LvYanfen JiangYufeng HouBihao LouHongchao ZhouYanming ZhangKangkang GuoTaylor & Francis Grouparticleclassical swine fever virusmir-140rab253ʹ utrinhibitionInfectious and parasitic diseasesRC109-216ENVirulence, Vol 11, Iss 1, Pp 260-269 (2020)
institution DOAJ
collection DOAJ
language EN
topic classical swine fever virus
mir-140
rab25
3ʹ utr
inhibition
Infectious and parasitic diseases
RC109-216
spellingShingle classical swine fever virus
mir-140
rab25
3ʹ utr
inhibition
Infectious and parasitic diseases
RC109-216
Panpan Xu
Shuangkai Jia
Kai Wang
Zhixin Fan
Hongqing Zheng
Jiangman Lv
Yanfen Jiang
Yufeng Hou
Bihao Lou
Hongchao Zhou
Yanming Zhang
Kangkang Guo
MiR-140 inhibits classical swine fever virus replication by targeting Rab25 in swine umbilical vein endothelial cells
description Classical swine fever virus (CSFV) is one of the most important viral pathogens leading worldwide threats to pig industry. MicroRNAs (miRNAs) play important roles in regulating virus replication, but whether miRNAs affect CSFV infection is still poorly understood. In previous study, we identified four miRNAs that were down-regulated by CSFV in swine umbilical vein endothelial cells (SUVEC). In this study, miR-140, one of the most potently down-regulated genes was investigated. We found that the miRNA expression was significantly inhibited by CSFV infection. Subsequent studies revealed that miR-140 mimics significantly inhibited CSFV replication, while the inhibition of endogenous miR-140 enhanced CSFV replication. By using bioinformatics prediction, luciferase reporter system, real-time fluorescence quantitative PCR (RT-qPCR) and Western blot assays, we further demonstrated that miR-140 bind to the 3ʹ UTR of Rab25 mRNA to regulate its expression. We also analyzed the expression pattern of Rab25 in SUVECs after CSFV infection. The results showed that CSFV infection induced Rab25 expression. Finally, Rab25 was found to promote CSFV replication. In conclusion, this study demonstrated that CSFV inhibits miR-140 expression and miR-140 inhibits replication by binding to host factor Rab25.
format article
author Panpan Xu
Shuangkai Jia
Kai Wang
Zhixin Fan
Hongqing Zheng
Jiangman Lv
Yanfen Jiang
Yufeng Hou
Bihao Lou
Hongchao Zhou
Yanming Zhang
Kangkang Guo
author_facet Panpan Xu
Shuangkai Jia
Kai Wang
Zhixin Fan
Hongqing Zheng
Jiangman Lv
Yanfen Jiang
Yufeng Hou
Bihao Lou
Hongchao Zhou
Yanming Zhang
Kangkang Guo
author_sort Panpan Xu
title MiR-140 inhibits classical swine fever virus replication by targeting Rab25 in swine umbilical vein endothelial cells
title_short MiR-140 inhibits classical swine fever virus replication by targeting Rab25 in swine umbilical vein endothelial cells
title_full MiR-140 inhibits classical swine fever virus replication by targeting Rab25 in swine umbilical vein endothelial cells
title_fullStr MiR-140 inhibits classical swine fever virus replication by targeting Rab25 in swine umbilical vein endothelial cells
title_full_unstemmed MiR-140 inhibits classical swine fever virus replication by targeting Rab25 in swine umbilical vein endothelial cells
title_sort mir-140 inhibits classical swine fever virus replication by targeting rab25 in swine umbilical vein endothelial cells
publisher Taylor & Francis Group
publishDate 2020
url https://doaj.org/article/ef501e4aca8841e1b79849b1c6b07bc3
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