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MicroRNA-based Regulation of Picornavirus Tropism
Published on: February 6, 2017
Integrated Analysis of miRNA-mRNA Expression in Mink Lung Epithelial Cells Infected With Canine Distemper Virus
Qiang Chen1,2,3, Mingwei Tong4, Na Sun5
1College of Veterinary Medicine, College of Animal Science and Technology, Jilin Agricultural University, Changchun, China.
Abstract:
Canine distemper (CD) caused by canine distemper virus (CDV) is one of the major infectious diseases in minks, bringing serious economic losses to the mink breeding industry. By an integrated analysis of microRNA (miRNA)-messenger RNA (mRNA), the present study analyzed the changes in the mink transcriptome upon CDV infection in mink lung epithelial cells (Mv. l. Lu cells) for the first time. A total of 4,734 differentially expressed mRNAs (2,691 upregulated and 2,043 downregulated) with |log2(FoldChange) |>1 and P-adj<0.05 and 181 differentially expressed miRNAs (152 upregulated and 29 downregulated) with |log2(FoldChange) |>2 and P-adj<0.05 were identified. Gene Ontology (GO) enrichment indicated that differentially expressed genes (DEGs) were associated with various biological processes and molecular function, such as response to stimulus, cell communication, signaling, cytokine activity, transmembrane signaling receptor activity and signaling receptor activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the combination of miRNA and mRNA was done for immune and inflammatory responses, such as Janus kinase (JAK)-signal transducer and activator (STAT) signaling pathway and nuclear factor (NF)-kappa B signaling pathway. The enrichment analysis of target mRNA of differentially expressed miRNA revealed that mir-140-5p and mir-378-12 targeted corresponding genes to regulate NF-kappa B signaling pathway. JAK-STAT signaling pathway could be modulated by mir-425-2, mir-139-4, mir-140-6, mir-145-3, mir-140-5p and mir-204-2. This study compared the influence of miRNA-mRNA expression in Mv. l. Lu cells before and after CDV infection by integrated analysis of miRNA-mRNA and analyzed the complex network interaction between virus and host cells. The results can help understand the molecular mechanism of the natural immune response induced by CDV infection in host cells.
Insights
Canine distemper virus (CDV) infection significantly alters mink lung cell gene and microRNA expression, impacting immune pathways like JAK-STAT and NF-kappa B. This research uncovers key molecular interactions in mink
Area of Science:
- Veterinary Virology
- Molecular Biology
- Immunology
Background:
- Canine distemper (CD) poses a significant threat to the mink industry, causing substantial economic losses.
- Understanding the molecular mechanisms of CDV infection in mink is crucial for disease management.
Purpose of the Study:
- To investigate the changes in microRNA (miRNA) and messenger RNA (mRNA) expression in mink lung cells following CDV infection.
- To identify key signaling pathways involved in the host response to CDV.
Main Methods:
- Integrated analysis of miRNA and mRNA sequencing data from CDV-infected mink lung epithelial cells (Mv. l. Lu).
- Differential gene and miRNA expression analysis, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis.
Main Results:
- Identification of 4,734 differentially expressed mRNAs and 181 differentially expressed miRNAs.
- Enrichment analysis revealed involvement in immune and inflammatory responses, including the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) and nuclear factor kappa B (NF-κB) signaling pathways.
- Specific miRNAs (e.g., mir-140-5p, mir-378-12, mir-425-2) were identified as regulators of these key immune pathways.
Conclusions:
- CDV infection induces complex miRNA-mRNA interactions in mink lung cells.
- The study elucidates the molecular basis of the host's innate immune response to CDV, highlighting the roles of JAK-STAT and NF-κB pathways.
- Findings provide insights into the pathogenesis of canine distemper in mink and potential targets for intervention.

