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miR-214-5p/C1QTNF1轴通过靶向AKT/mTOR信号通路促进自噬来增强猪圆环病毒2型(PCV2)的复制。

miR-214-5p/C1QTNF1 axis enhances PCV2 replication through promoting autophagy by targeting AKT/mTOR signaling pathway.

作者信息

Cao Yue, Jing Pengfei, Yu Luchen, Wu Zhengchang, Gao Song, Bao Wenbin

机构信息

Key Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design of Jiangsu Province, College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China.

Key Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design of Jiangsu Province, College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China; College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China.

出版信息

Virus Res. 2023 Jan 2;323:198990. doi: 10.1016/j.virusres.2022.198990. Epub 2022 Oct 24.

DOI:10.1016/j.virusres.2022.198990
PMID:36302471
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10194317/
Abstract

Porcine circovirus type 2 (PCV2) is the causative agent of PCV2-associated disease, which causes a relevant economic impact on the global swine industry. Accumulating data have indicated host microRNAs play essential roles in numerous virus replication of pigs, while their roles in PCV2 replication remain unclear. Herein, we demonstrated that PCV2 infection downregulated the expression of miR-214-5p in PK15 cells, and miR-214-5p promoted PCV2 replication. C1q/tumor necrosis factor-related protein 1 (C1QTNF1) was then identified as a target gene of miR-214-5p, and C1QTNF1 suppressed PCV2 replication. Interestingly, miR-214-5p/C1QTNF1 axis negatively regulated AKT/mTOR signaling, and then enhanced PCV2 replication through promoting autophagy in PK15 cells. Collectively, our findings provide insight into the mechanism of PCV2 replication and highlight miR-214-5p and C1QTNF1 as potential novel targets for the treatment of PCV2 infection.

摘要

猪圆环病毒2型(PCV2)是与PCV2相关疾病的病原体,对全球养猪业造成了重大经济影响。越来越多的数据表明,宿主微小RNA在猪的多种病毒复制中起着至关重要的作用,但其在PCV2复制中的作用仍不清楚。在此,我们证明PCV2感染下调了PK15细胞中miR-214-5p的表达,且miR-214-5p促进了PCV2的复制。随后,C1q/肿瘤坏死因子相关蛋白1(C1QTNF1)被鉴定为miR-214-5p的靶基因,C1QTNF1抑制PCV2复制。有趣的是,miR-214-5p/C1QTNF1轴负向调节AKT/mTOR信号通路,进而通过促进PK15细胞中的自噬增强PCV2复制。总之,我们的研究结果为PCV2复制机制提供了见解,并突出了miR-214-5p和C1QTNF1作为治疗PCV2感染潜在新靶点的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/a8fda79c1b25/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/0c3d2c8e92e3/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/d36b6fe81698/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/323baafe9622/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/ea9412e0c1cb/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/767d99e653cc/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/a8fda79c1b25/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/0c3d2c8e92e3/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/d36b6fe81698/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/323baafe9622/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/ea9412e0c1cb/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/767d99e653cc/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d9/10194317/a8fda79c1b25/gr6.jpg

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