ArticleViruses2014
Japanese encephalitis virus upregulates the expression of SOCS3 in mouse brain and Raw264.7 Cells.
Article in Viruses, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- ZIKV Strains Elicit Different Inflammatory and Anti-Viral Responses in Microglia Cells.Viruses · 2023Article
- Neurotropic RNA Virus Modulation of Immune Responses within the Central Nervous System.International journal of molecular sciences · 2022Review
- Coxsackievirus B3 Infection of Human Neural Progenitor Cells Results in Distinct Expression Patterns of Innate Immune Genes.Viruses · 2020Article
- Zika Virus-Induction of the Suppressor of Cytokine Signaling 1/3 Contributes to the Modulation of Viral Replication.Pathogens (Basel, Switzerland) · 2020Article
- Stem cell persistence in CML is mediated by extrinsically activated JAK1-STAT3 signaling.Leukemia · 2019Article
- CD8 T cells protect adult naive mice from JEV-induced morbidity via lytic function.PLoS neglected tropical diseases · 2017Article
- Japanese Encephalitis Virus exploits the microRNA-432 to regulate the expression of Suppressor of Cytokine Signaling (SOCS) 5.Scientific reports · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Japanese encephalitis virus (JEV) is one of the pathogens that can invade the central nervous system, causing acute infection and inflammation of brain. SOCS3 protein plays a vital role in immune processes and inflammation of the central nervous system. In this study, Raw264.7 cells and suckling mice were infected with JEV, and SOCS3 expression was analyzed by the gene expression profile, semiquantitative RT-PCR, qRT-PCR, immunohistochemistry (IHC) and Western blot. Results indicated that 520 genes were found to be differentially expressed (fold change ≥ 2.0, p < 0.05) in total. The differentially regulated genes were involved in biological processes, such as stimulus response, biological regulation and immune system processes. JEV early infection could induce SOCS3 expression, upregulating both the mRNA and protein levels in Raw264.7 cells in a time-dependent manner. The SOCS3 expression was much lower in Raw264.7 cells infected with inactivated JEV than wild-type JEV. In vivo, SOCS3 protein was also found to upregulate the expression of mRNA and protein in JEV-infected mouse brain. Taken together, our data showed that JEV early infection could induce the upregulation of SOCS3 expression, both in vitro and in vivo, providing the basic theoretical foundation for future research on the invasion mechanism of JEV.
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