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微小RNA-127-5p通过直接靶向SCARB2负向调控肠道病毒71型的复制。

miR-127-5p negatively regulates enterovirus 71 replication by directly targeting SCARB2.

作者信息

Feng Chunhong, Fu Yuxuan, Chen Deyan, Wang Huanru, Su Airong, Zhang Li, Chang Liang, Zheng Nan, Wu Zhiwei

机构信息

Center for Public Health Research Medical School Nanjing University China.

School of life sciences Nanjing University China.

出版信息

FEBS Open Bio. 2017 Apr 13;7(6):747-758. doi: 10.1002/2211-5463.12197. eCollection 2017 Jun.

DOI:10.1002/2211-5463.12197
PMID:28593131
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5458453/
Abstract

Enterovirus 71 (EV71) is the major causative agent of hand-foot-and-mouth disease in young children and can cause severe cerebral and pulmonary complications and even fatality. This study aimed at elucidating whether and how EV71 infection is regulated by a cellular microRNA, miR-127-5p. We found that miR-127-5p can downregulate the expression of SCARB2, a main receptor of EV71, by targeting two potential sites in its 3' UTR region and inhibit EV71 infection. Meanwhile, miR-127-5p expression was upregulated during EV71 infection. Notably, transfecting cells with miR-127-5p mimics led to a significant decrease in viral replication, while inhibition of endogenous miR-127-5p facilitated viral replication. Furthermore, our evidence showed that miR-127-5p did not affect postentry viral replication. Taken together, these results indicated that miR-127-5p inhibited EV71 replication by targeting the SCARB2 mRNA.

摘要

肠道病毒71型(EV71)是幼儿手足口病的主要致病原,可引发严重的脑和肺部并发症,甚至导致死亡。本研究旨在阐明EV71感染是否以及如何受细胞微小RNA miR-127-5p调控。我们发现,miR-127-5p可通过靶向其3'UTR区域的两个潜在位点下调EV71的主要受体SCARB2的表达,并抑制EV71感染。同时,在EV71感染期间miR-127-5p表达上调。值得注意的是,用miR-127-5p模拟物转染细胞导致病毒复制显著减少,而抑制内源性miR-127-5p则促进病毒复制。此外,我们的证据表明,miR-127-5p不影响病毒进入后的复制。综上所述,这些结果表明miR-127-5p通过靶向SCARB2 mRNA抑制EV71复制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/0c6c353d56fd/FEB4-7-747-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/d8b5b128645e/FEB4-7-747-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/c72729d6987e/FEB4-7-747-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/10577b65cfc8/FEB4-7-747-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/22d71d1a0fac/FEB4-7-747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/0c6c353d56fd/FEB4-7-747-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/d8b5b128645e/FEB4-7-747-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/c72729d6987e/FEB4-7-747-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/10577b65cfc8/FEB4-7-747-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/22d71d1a0fac/FEB4-7-747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da8/5458453/0c6c353d56fd/FEB4-7-747-g005.jpg

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