SP1/miR-92a-1-5p/SOCS5: A novel regulatory axis in feline panleukopenia virus replication

被引:4
|
作者
Liang, Ruiying [1 ]
Liang, Lin [1 ]
Zhao, Jingjie [1 ]
Liu, Weiquan [3 ]
Cui, Shangjin [1 ]
Zhang, Xinglin [2 ]
Zhang, Lingling [2 ]
机构
[1] Chinese Acad Agr Sci, Inst Anim Sci, Beijing 100193, Peoples R China
[2] Linyi Univ, Inst Microbe & Host Hlth, Linyi 276005, Shandong, Peoples R China
[3] China Agr Univ, Coll Biol Sci, Dept Biochem & Mol Biol, State Key Lab Agrobiotechnol, Beijing 100193, Peoples R China
基金
中国国家自然科学基金;
关键词
FPV; MiR-92a-1-5p; SP1; SOCS5; Type I interferons; MICRORNA BIOGENESIS PATHWAYS; RESPIRATORY SYNDROME VIRUS; PROTEIN EXPRESSION; SMALL RNAS; INFECTION; RESPONSES; INNATE; SUPPRESSION; MODULATION; ENCODES;
D O I
10.1016/j.vetmic.2022.109549
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
MicroRNAs (miRNAs) are vital post-transcriptional regulators that participate in host-pathogen interactions by modulating the expression of cellular factors. Previous studies have demonstrated that feline panleukopenia virus (FPV) alters miRNA expression levels within host cells. However, the relationship between FPV replication and host miRNAs remains unclear. Here, we demonstrated that FPV infection significantly altered cellular miR-92a1-5p expression in F81 cells by upregulating the expression of specificity protein 1 (SP1). Furthermore, we observed that miR-92a-1-5p enhanced interferon (IFN-alpha/ss) expression by targeting the suppressors of cytokine signaling 5 (SOCS5) that negatively regulates NF-.B signaling and inhibits FPV replication in host cells. These findings revealed that miR-92a-1-5p plays a crucial role in host defense against FPV infection.
引用
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页数:13
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