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The regulatory role of miR-107 in Coxsackie B3 virus replication
Coxsackie B3 virus (CVB3) is a member of small RNA viruses that belongs to the genus Enterovirus of the family Picornaviridae and CVB3 is the main pathogen of acute and chronic viral myocarditis. In this study RT-qPCR was used to determine the expression of miR-107 in CVB3-infected and uninfected He...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425430/ https://www.ncbi.nlm.nih.gov/pubmed/32674073 http://dx.doi.org/10.18632/aging.103488 |
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author | Yao, Min Xu, Chi Shen, Hongxing Liu, Tingjun Wang, Xiuping Shao, Chen Shao, Shihe |
author_facet | Yao, Min Xu, Chi Shen, Hongxing Liu, Tingjun Wang, Xiuping Shao, Chen Shao, Shihe |
author_sort | Yao, Min |
collection | PubMed |
description | Coxsackie B3 virus (CVB3) is a member of small RNA viruses that belongs to the genus Enterovirus of the family Picornaviridae and CVB3 is the main pathogen of acute and chronic viral myocarditis. In this study RT-qPCR was used to determine the expression of miR-107 in CVB3-infected and uninfected HeLa cells. The experimental results show that the level of miR-107 began to rise at 4 h after the infection, and significantly boosted at 6 h. Based on the results of this experiment, we consider that miR-107 expression is related to CVB3 infection. In order to further clarify the effect of miR-107 in the process of CVB3 infection, we studied the effect of miR-107 upstream and downstream target genes on CVB3 replication. Levels of the target RNAs were detected by RT-qPCR after CVB3 infection, and the expression of CVB3 capsid protein VP1 by western blot analysis. Then the virus in the supernatant was quantitated via a viral plaque assay, reflecting the release of the virus. The experimental results showed that miRNA-107 expression is associated with CVB3 replication and proliferation, while KLF4 and BACE1 as the downstream of miR-107 weakened CVB3 replication. Overexpressions of KLF4 and BACE1 negatively regulated CVB3 replication, this effect on CVB3 was completely opposite to that of miR-107. Further experiments revealed that the upstream lncRNA004787, a new lncRNA that had not been reported, was located on chromosome 5, strand - from 37073250 to 37070908 (genome assembly: hg19). We sequenced and studied lncRNA004787 and found that it partially inhibited CVB3 replication. This prompted us to speculate that lncRNA004787 probably impacted the replication by other means. In conclusion, miR-107 interfered with CVB3 replication and release. |
format | Online Article Text |
id | pubmed-7425430 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-74254302020-08-25 The regulatory role of miR-107 in Coxsackie B3 virus replication Yao, Min Xu, Chi Shen, Hongxing Liu, Tingjun Wang, Xiuping Shao, Chen Shao, Shihe Aging (Albany NY) Research Paper Coxsackie B3 virus (CVB3) is a member of small RNA viruses that belongs to the genus Enterovirus of the family Picornaviridae and CVB3 is the main pathogen of acute and chronic viral myocarditis. In this study RT-qPCR was used to determine the expression of miR-107 in CVB3-infected and uninfected HeLa cells. The experimental results show that the level of miR-107 began to rise at 4 h after the infection, and significantly boosted at 6 h. Based on the results of this experiment, we consider that miR-107 expression is related to CVB3 infection. In order to further clarify the effect of miR-107 in the process of CVB3 infection, we studied the effect of miR-107 upstream and downstream target genes on CVB3 replication. Levels of the target RNAs were detected by RT-qPCR after CVB3 infection, and the expression of CVB3 capsid protein VP1 by western blot analysis. Then the virus in the supernatant was quantitated via a viral plaque assay, reflecting the release of the virus. The experimental results showed that miRNA-107 expression is associated with CVB3 replication and proliferation, while KLF4 and BACE1 as the downstream of miR-107 weakened CVB3 replication. Overexpressions of KLF4 and BACE1 negatively regulated CVB3 replication, this effect on CVB3 was completely opposite to that of miR-107. Further experiments revealed that the upstream lncRNA004787, a new lncRNA that had not been reported, was located on chromosome 5, strand - from 37073250 to 37070908 (genome assembly: hg19). We sequenced and studied lncRNA004787 and found that it partially inhibited CVB3 replication. This prompted us to speculate that lncRNA004787 probably impacted the replication by other means. In conclusion, miR-107 interfered with CVB3 replication and release. Impact Journals 2020-07-16 /pmc/articles/PMC7425430/ /pubmed/32674073 http://dx.doi.org/10.18632/aging.103488 Text en Copyright © 2020 Yao et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Yao, Min Xu, Chi Shen, Hongxing Liu, Tingjun Wang, Xiuping Shao, Chen Shao, Shihe The regulatory role of miR-107 in Coxsackie B3 virus replication |
title | The regulatory role of miR-107 in Coxsackie B3 virus replication |
title_full | The regulatory role of miR-107 in Coxsackie B3 virus replication |
title_fullStr | The regulatory role of miR-107 in Coxsackie B3 virus replication |
title_full_unstemmed | The regulatory role of miR-107 in Coxsackie B3 virus replication |
title_short | The regulatory role of miR-107 in Coxsackie B3 virus replication |
title_sort | regulatory role of mir-107 in coxsackie b3 virus replication |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425430/ https://www.ncbi.nlm.nih.gov/pubmed/32674073 http://dx.doi.org/10.18632/aging.103488 |
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