ArticleCellular and molecular life sciences : CMLS2013
MicroRNA-203 enhances coxsackievirus B3 replication through targeting zinc finger protein-148.
Article in Cellular and molecular life sciences : CMLS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 52 citations in OpenAlex.
- Review
- The dual actions of miRNA16a in restricting Bovine Coronavirus replication through downregulation of Furin and enhancing the host immune response.Scientific reports · 2024Article
- The Role of MicroRNA in the Pathophysiology and Diagnosis of Viral Myocarditis.International journal of molecular sciences · 2024Review
- MicroRNA delivery based on nanoparticles of cardiovascular diseases.Molecular and cellular biochemistry · 2024Review
- Infectious factors in myocarditis: a comprehensive review of common and rare pathogens.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024Review
- MicroRNA-22-3p displaces critical host factors from the 5' UTR and inhibits the translation of Coxsackievirus B3 RNA.Journal of virology · 2024Article
- MicroRNAs in Myocarditis-Review of the Preclinical In Vivo Trials.Biomedicines · 2023Review
- The role of non-coding RNAs in myocarditis: a narrative review.Annals of translational medicine · 2022Review
- Essential Role of Non-Coding RNAs in Enterovirus Infection: From Basic Mechanisms to Clinical Prospects.International journal of molecular sciences · 2021Review
- Weighted gene co-expression network analysis identified underlying hub genes and mechanisms in the occurrence and development of viral myocarditis.Annals of translational medicine · 2020Article
- The Role of Non-coding RNAs in Viral Myocarditis.Frontiers in cellular and infection microbiology · 2020Review
- Dysregulated CD4+ T Cells and microRNAs in Myocarditis.Frontiers in immunology · 2020Review
- Construction of miRNA-target networks using microRNA profiles of CVB3-infected HeLa cells.Scientific reports · 2019Article
- Review
- Up-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR1.Scientific reports · 2018Article
- Detecting TF-miRNA-gene network based modules for 5hmC and 5mC brain samples: a intra- and inter-species case-study between human and rhesus.BMC genetics · 2018Article
- MicroRNA-20b suppresses the expression of ZFP-148 in viral myocarditis.Molecular and cellular biochemistry · 2017Article
- MicroRNAs in Type 1 Diabetes: Complex Interregulation of the Immune System, β Cell Function and Viral Infections.Current diabetes reports · 2016Review
- Microarray analysis reveals altered circulating microRNA expression in mice infected with Coxsackievirus B3.Experimental and therapeutic medicine · 2016Article
- MicroRNA and Pathogenesis of Enterovirus Infection.Viruses · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coxsackievirus B3 (CVB3) is the primary causal agent of viral myocarditis. During infection, it hijacks host genes to favour its own replication. However, the underlying mechanism is still unclear. Although the viral receptor is an important factor for viral infectivity, other factors such as microRNAs (miRNA) may also play an essential role in its replication after host cell entry. miRNAs are post-transcriptional gene regulators involved in various fundamental biological processes as well as in diseases. To identify miRNAs involved in CVB3 pathogenesis, we performed microarray analysis of miRNAs using CVB3-infected murine hearts and identified miR-203 as one of the most upregulated candidates. We found that miR-203 upregulation is through the activation of protein kinase C/transcription factor AP-1 pathway. We further identified zinc finger protein-148 (ZFP-148), a transcription factor, as a novel target of miR-203. Ectopic expression of miR-203 downregulated ZFP-148 translation, increased cell viability and subsequently enhanced CVB3 replication. Silencing of ZFP-148 by siRNA showed similar effects on CVB3 replication. Finally, analyses of the signalling cascade downstream of ZFP-148 revealed that miR-203-induced suppression of ZFP-148 differentially regulated the expression of prosurvival and proapoptotic genes of the Bcl-2 family proteins as well as the cell cycle regulators. This altered gene expression promoted cell survival and growth, which provided a favourable environment for CVB3 replication, contributing to the further damage of the infected cells. Taken together, this study identified a novel target of miR-203 and revealed, for the first time, the molecular link between miR-203/ZFP-148 and the pathogenesis of CVB3.
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