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Effect of miR-155 on type I interferon response in Epithelioma papulosum cyprini cells
1Department of Aquatic Life Medicine, Pukyong National University, Busan, 48513, South Korea.
Abstract:
MicroRNA-155 (miRNA-155) is known to play an important role in the regulation of innate and adaptive immune responses in mammals. However, no information is available on the role of miRNA-155 in relation to type I interferon (IFN) responses in fish cells. In the present study, we found that the protein inhibitor of activated STAT 4a (PIAS4a) gene of fathead minnow (Pimephales promelas) was a target of miR-155, which was verified by the inhibitory activity of miR-155 in the expression of reporter gene harboring 3'UTR of PIAS4a of EPC cells. Furthermore, cells over-expressing miR-155 showed a significantly higher type I IFN response after polyinosinic-polycytidylic acid (poly I:C) stimulation, suggesting the targeting of PIAS4a in EPC cells by miR-155 can be a cause of the up-regulation of type I IFN, and miR-155 can act as an antiviral factor. However, as the targeting PIAS4a might not be the sole cause of the type I IFN up-regulation by miR-155, further studies on the uncovering of miR-155 target genes that are involved in type I IFN responses in fish are required.
Insights
MicroRNA-155 (miRNA-155) targets PIAS4a in fish cells, enhancing type I interferon responses. This suggests miRNA-155 acts as an antiviral factor, crucial for innate immunity in aquatic species.
Area of Science:
- Immunology
- Molecular Biology
- Aquatic Animal Health
Background:
- MicroRNA-155 (miRNA-155) regulates immune responses in mammals.
- The role of miRNA-155 in fish type I interferon (IFN) responses remains uncharacterized.
Purpose of the Study:
- Investigate the function of miRNA-155 in fish immune cells.
- Determine if miRNA-155 influences type I interferon production in fathead minnow (Pimephales promelas).
Main Methods:
- Utilized reporter gene assays to confirm PIAS4a as a miRNA-155 target in EPC cells.
- Over-expressed miRNA-155 in fish cells and stimulated with polyinosinic-polycytidylic acid (poly I:C).
- Quantified type I IFN responses following miRNA-155 manipulation and stimulation.
Main Results:
- Confirmed PIAS4a gene as a direct target of miRNA-155 in fathead minnow cells.
- Cells over-expressing miRNA-155 exhibited significantly elevated type I IFN responses after poly I:C stimulation.
- Demonstrated that miRNA-155 targeting of PIAS4a contributes to type I IFN up-regulation.
Conclusions:
- miRNA-155 plays a role in modulating type I IFN responses in fish.
- miRNA-155 functions as an antiviral factor in fish by targeting PIAS4a.
- Further research is needed to identify additional miRNA-155 targets involved in fish antiviral immunity.
