HnRNPM inhibits pseudorabies virus replication by inducing apoptosis in infected cells

IF 2.4 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology Pub Date : 2025-03-04 DOI:10.1016/j.vetmic.2025.110455

Xiaoxiao Zhao , Yan Qiao , Songjie Fan , Xiaotian Chang , Jiafu Zhao , Kai Zhong , Yingqian Han , Heshui Zhu , Chao Zhang

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引用次数: 0

Abstract

Heterogeneous nuclear ribonucleoproteins (hnRNPs) are a family of RNA-binding proteins that play crucial roles in RNA processing, transcriptional regulation, nucleocytoplasmic transport, and apoptosis. As a member of the hnRNP family, heterogeneous nuclear ribonucleoprotein M (hnRNPM) has been implicated in diverse cellular processes, including the regulation of tumor-associated gene expression, promotion of angiogenesis, enhancement of tumor cell invasion and metastasis, and modulation of RNA virus replication. However, the interaction between hnRNPM and pseudorabies virus (PRV) remains unexplored. In this study, we demonstrated that hnRNPM overexpression in PK15 and 3D4/21 cells significantly inhibited PRV replication, whereas hnRNPM knockdown enhanced viral replication. Although PRV infection did not alter total cellular hnRNPM levels, it induced the nuclear translocation of hnRNPM. Mechanistically, hnRNPM promoted apoptosis in PRV-infected cells by upregulating the expression of cleaved caspase-3, −6, and −7, as well as Bax, while downregulating Bcl-2. This apoptosis induction consequently suppressed PRV replication. Furthermore, hnRNPM was found to colocalize with caspase-6. Our findings reveal that hnRNPM inhibits PRV replication by inducing apoptosis in infected cells. These results not only enhance our understanding of PRV-host interactions but also highlight hnRNPM as a promising therapeutic target for the development of antiviral strategies against PRV.

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来源期刊

Veterinary microbiology 农林科学-兽医学

CiteScore

5.90

自引率

6.10%

发文量

221

审稿时长

52 days

期刊介绍： Veterinary Microbiology is concerned with microbial (bacterial, fungal, viral) diseases of domesticated vertebrate animals (livestock, companion animals, fur-bearing animals, game, poultry, fish) that supply food, other useful products or companionship. In addition, Microbial diseases of wild animals living in captivity, or as members of the feral fauna will also be considered if the infections are of interest because of their interrelation with humans (zoonoses) and/or domestic animals. Studies of antimicrobial resistance are also included, provided that the results represent a substantial advance in knowledge. Authors are strongly encouraged to read - prior to submission - the Editorials (''Scope or cope'' and ''Scope or cope II'') published previously in the journal. The Editors reserve the right to suggest submission to another journal for those papers which they feel would be more appropriate for consideration by that journal. Original research papers of high quality and novelty on aspects of control, host response, molecular biology, pathogenesis, prevention, and treatment of microbial diseases of animals are published. Papers dealing primarily with immunology, epidemiology, molecular biology and antiviral or microbial agents will only be considered if they demonstrate a clear impact on a disease. Papers focusing solely on diagnostic techniques (such as another PCR protocol or ELISA) will not be published - focus should be on a microorganism and not on a particular technique. Papers only reporting microbial sequences, transcriptomics data, or proteomics data will not be considered unless the results represent a substantial advance in knowledge. Drug trial papers will be considered if they have general application or significance. Papers on the identification of microorganisms will also be considered, but detailed taxonomic studies do not fall within the scope of the journal. Case reports will not be published, unless they have general application or contain novel aspects. Papers of geographically limited interest, which repeat what had been established elsewhere will not be considered. The readership of the journal is global.