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微小RNA-23b通过靶向干扰素调节因子1促进禽白血病病毒J亚群(ALV-J)复制。

MicroRNA-23b Promotes Avian Leukosis Virus Subgroup J (ALV-J) Replication by Targeting IRF1.

作者信息

Li Zhenhui, Chen Biao, Feng Min, Ouyang Hongjia, Zheng Ming, Ye Qiao, Nie Qinghua, Zhang Xiquan

机构信息

1] Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou 510642, Guangdong, China [2] Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Lab of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou 510642, Guangdong, China.

出版信息

Sci Rep. 2015 May 18;5:10294. doi: 10.1038/srep10294.

DOI:10.1038/srep10294
PMID:25980475
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4434839/
Abstract

Avian leukosis virus subgroup J (ALV-J) can cause several different leukemia-like proliferative diseases in the hemopoietic system of chickens. Here, we investigated the transcriptome profiles and miRNA expression profiles of ALV-J-infected and uninfected chicken spleens to identify the genes and miRNAs related to ALV-J invasion. In total, 252 genes and 167 miRNAs were differentially expressed in ALV-J-infected spleens compared to control uninfected spleens. miR-23b expression was up-regulated in ALV-J-infected spleens compared with the control spleens, and transcriptome analysis revealed that the expression of interferon regulatory factor 1 (IRF1) was down-regulated in ALV-J-infected spleens compared to uninfected spleens. A dual-luciferase reporter assay showed that IRF1 was a direct target of miR-23b. miR-23b overexpression significantly (P = 0.0022) decreased IRF1 mRNA levels and repressed IRF1-3'-UTR reporter activity. In vitro experiments revealed that miR-23b overexpression strengthened ALV-J replication, whereas miR-23b loss of function inhibited ALV-J replication. IRF1 overexpression inhibited ALV-J replication, and IRF1 knockdown enhanced ALV-J replication. Moreover, IRF1 overexpression significantly (P = 0.0014) increased IFN-β expression. In conclusion, these results suggested that miR-23b may play an important role in ALV-J replication by targeting IRF1.

摘要

禽白血病病毒J亚群(ALV-J)可在鸡的造血系统中引发几种不同的白血病样增殖性疾病。在此,我们研究了ALV-J感染和未感染鸡脾脏的转录组图谱和miRNA表达谱,以鉴定与ALV-J入侵相关的基因和miRNA。与未感染的对照脾脏相比,ALV-J感染的脾脏中共有252个基因和167个miRNA差异表达。与对照脾脏相比,miR-23b在ALV-J感染的脾脏中表达上调,转录组分析显示,与未感染的脾脏相比,干扰素调节因子1(IRF1)在ALV-J感染的脾脏中表达下调。双荧光素酶报告基因检测表明IRF1是miR-23b的直接靶标。miR-23b过表达显著(P = 0.0022)降低IRF1 mRNA水平并抑制IRF1-3'-UTR报告基因活性。体外实验表明,miR-23b过表达增强了ALV-J复制,而miR-23b功能缺失则抑制了ALV-J复制。IRF1过表达抑制ALV-J复制,而IRF1敲低增强ALV-J复制。此外,IRF1过表达显著(P = 0.0014)增加IFN-β表达。总之,这些结果表明miR-23b可能通过靶向IRF1在ALV-J复制中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/6fee2ae19d8f/srep10294-f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/35c101dc6dea/srep10294-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/0da5c5eaacb7/srep10294-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/6fee2ae19d8f/srep10294-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/f573a7b1d2f0/srep10294-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/239f54150d74/srep10294-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/bd8be8e167a6/srep10294-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/d6649f9c7ec2/srep10294-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/35c101dc6dea/srep10294-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/0da5c5eaacb7/srep10294-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f452/4434839/6fee2ae19d8f/srep10294-f7.jpg

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