ArticleNeurochemical research2020
Impaired Autophagy Flux is Associated with Proinflammatory Microglia Activation Following Japanese Encephalitis Virus Infection.
Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Frequency and Focus of in Vitro Studies of Microglia-Expressed Cytokines in Response to Viral Infection: A Systematic Review.Cellular and molecular neurobiology · 2024Pooled it
- Targeting canonical TGFβ/SMAD3 and ERK1/2 signaling in human valve interstitial cells to modulate immune-fibrotic responses in rheumatic heart disease.Journal of physiology and biochemistry · 2026Article
- Targeting phospholipase A2 with arachidonyl trifluoromethyl ketone modulates macrophage activation during Japanese encephalitis virus infection.Medical microbiology and immunology · 2026Article
- VPS34-mediated autophagosome-lysosome fusion facilitates classical swine fever virus replication.Journal of virology · 2025Article
- NMDA receptor blockade attenuates Japanese encephalitis virus infection-induced microglia activation.Journal of neuroinflammation · 2024Article
- Intracellular Iron Accumulation Induces Inflammatory and Oxidative Status of the Host After Japanese Encephalitis Viral Infection.Molecular neurobiology · 2024Article
- Mechanisms of ferroptosis and the relationship between ferroptosis and ER stress after JEV and HSV infection.Frontiers in microbiology · 2024Review
- Duck Tembusu virus induces incomplete autophagy via the ERK/mTOR and AMPK/mTOR signalling pathways to promote viral replication in neuronal cells.Veterinary research · 2023Article
- Japanese Encephalitis Virus Infection Causes an Imbalance in the Activation of Mitochondrial Fusion/Fission Genes and Triggers the Activation of NOX2-mediated Oxidative Stress and Neuronal Cell Death.Neurochemical research · 2023Article
- Deep Proteomics Network and Machine Learning Analysis of Human Cerebrospinal Fluid in Japanese Encephalitis Virus Infection.Journal of proteome research · 2023Article
- Exaggerated levels of some specific TLRs, cytokines and chemokines in Japanese encephalitis infected BV2 and neuro 2A cell lines associated with worst outcome.Virology journal · 2023Article
- Functional Analysis of the Cathepsin D Gene Response to SGIV Infection in the Orange-Spotted Grouper,Viruses · 2022Article
- Impairment of autophagy after spinal cord injury potentiates neuroinflammation and motor function deficit in mice.Theranostics · 2022Article
- Lipopolysaccharide-Induced Microglial Neuroinflammation: Attenuation by FK866.Neurochemical research · 2021Article
- The Role of Microglia during West Nile Virus Infection of the Central Nervous System.Vaccines · 2020Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Role of autophagy in Japanese encephalitis viral (JEV) infection is not well known. In the present study, we reported the role of autophagy flux in microglia activation, neurobehavioral function and neuronal death using a mouse model of JEV. Markers for autophagy (LC3-II/I, SQSTM1/P62, phos-Akt, phos-AMPK), and neuronal death (cleaved caspase 12, H2Ax, polyubiquitin) were investigated by western blot at 1, 3 and 7 days post inoculation. Cathepsin D was measured in cerebral cotex of JEV infected mice spectrophotometrically. Microglia activation and pro-inflammatory cytokines (IL1β, TNF-α, IFNγ, IL6) were measured by immunohistochemistry, western blot and qPCR analysis. In order to determine the neuroinflammatory changes and autophagy mediated neuronal cell death, BV2-microglia and N2a-neuronal cells were used. Autophagy activation marker LC3-II/I and its substrate SQSTM1/P62 were significantly increased while cathepsin D activity was decreased on day 7 post inoculation in cerebral cortex. Microglia in cortex were activated and showed higher expression of proinflammatory mRNA of IL1β, TNF-α, IFNγ and IL6, with increased DNA damage (H2AX) and neuronal cell death pathways in hippocampus and neurobehavioral dysfunction. Similar observations on JEV infection mediated autophagy flux inhibition and neuronal cell death was found in N2a neuronal cell. Collectively, our study provides evidence on the role of autophagy regulation, microglial activation and neurodegeneration following JEV infection.
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Registered trials
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