Both MicroRNA-155 and Virus-Encoded MiR-155 Ortholog Regulate TLR3 Expression

被引:58
作者
Hu, Xuming [1 ,2 ]
Ye, Jianqiang [1 ,3 ]
Qin, Aijian [1 ,2 ,3 ]
Zou, Haitao [2 ,3 ]
Shao, Hongxia [1 ,2 ,3 ]
Qian, Kun [1 ,2 ,3 ]
机构
[1] Yangzhou Univ, Key Lab Avian Prevent Med, Minist Educ, Yangzhou 225009, Jiangsu, Peoples R China
[2] Yangzhou Univ, Key Lab Jiangsu Prevent Vet Med, Yangzhou 225009, Jiangsu, Peoples R China
[3] Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Jiangsu, Peoples R China
来源
PLOS ONE | 2015年 / 10卷 / 05期
基金
中国国家自然科学基金;
关键词
T-CELL RESPONSES; CODING REGIONS; TARGETING SOCS1; CUTTING EDGE; MICRO-RNA; IMMUNITY; CONTRIBUTES; SUPPRESSION; DEFICIENCY; ACTIVATION;
D O I
10.1371/journal.pone.0126012
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
MicroRNA-155 (miR-155) has been as an important controller of TLR3 signalling. However, the interactions between miR-155 and TLR3 are poorly understood. Here, we focused on the regulation of the relationship between miR-155 and TLR3. Sequence analyses and firefly luciferase reporter assay revealed that miR-155 target were present in the coding sequences (CDS) of TLR3. And the expression of the TLR3 protein could be inhibited by a miR-155 mimic or by a virally encoded orthologue in chick embryo fibroblast cells. Notably, endogenous miR-155 induction emerged a negative regulation on TLR3 expression in TLR2, 4 and 7 ligands stimulated HD11 cells, an avian macrophage cell line. Moreover, treatment with the miR-155 antagomir increased TLR3 levels while significantly decreased the abundance of TLR3 with miR-155 agomir. In addition, our data showed that miR-155 could inhibit IFN-beta production possibly though TLR3 signal pathway. All these findings might reveal a new mechanism by which miR-155 can regulate the TLR3 immune response.
引用
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页数:13
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