ArticleJournal of neuroinflammation2014
Type-1 interferons contribute to oxygen glucose deprivation induced neuro-inflammation in BE(2)M17 human neuroblastoma cells.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Immune Response in Traumatic Brain Injury.Current neurology and neuroscience reports · 2024Review
- Mitochondrial DNA leakage triggers inflammation in age-related cardiovascular diseases.Frontiers in cell and developmental biology · 2024Review
- Resveratrol Mitigates Oxygen and Glucose Deprivation-Induced Inflammation, NLRP3 Inflammasome, and Oxidative Stress in 3D Neuronal Culture.International journal of molecular sciences · 2022Article
- The critical roles of histone deacetylase 3 in the pathogenesis of solid organ injury.Cell death & disease · 2021Review
- Identifying the pattern of immune related cells and genes in the peripheral blood of ischemic stroke.Journal of translational medicine · 2020Article
- HDAC3 inhibition ameliorates ischemia/reperfusion-induced brain injury by regulating the microglial cGAS-STING pathway.Theranostics · 2020Article
- High-throughput screening for small molecule inhibitors of the type-I interferon signaling pathway.Acta pharmaceutica Sinica. B · 2018Article
- The Nox1/Nox4 inhibitor attenuates acute lung injury induced by ischemia-reperfusion in mice.PloS one · 2018Article
- Interferons in Traumatic Brain and Spinal Cord Injury: Current Evidence for Translational Application.Frontiers in neurology · 2018Review
- Sodium hydrosulfide attenuates cerebral ischemia/reperfusion injury by suppressing overactivated autophagy in rats.FEBS open bio · 2017Article
- RIG-I contributes to the innate immune response after cerebral ischemia.Journal of inflammation (London, England) · 2015Article
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5 authors.
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Abstract
backgroundHypoxic-ischaemic injuries such as stroke and traumatic brain injury exhibit features of a distinct neuro-inflammatory response in the hours and days post-injury. Microglial activation, elevated pro-inflammatory cytokines and macrophage infiltration contribute to core tissue damage and contribute to secondary injury within a region termed the penumbra. Type-1 interferons (IFNs) are a super-family of pleiotropic cytokines that regulate pro-inflammatory gene transcription via the classical Jak/Stat pathway; however their role in hypoxia-ischaemia and central nervous system neuro-inflammation remains unknown. Using an in vitro approach, this study investigated the role of type-1 IFN signalling in an inflammatory setting induced by oxygen glucose deprivation (OGD).
methodsHuman BE(2)M17 neuroblastoma cells or cells expressing a type-1 interferon-α receptor 1 (IFNAR1) shRNA or negative control shRNA knockdown construct were subjected to 4.5 h OGD and a time-course reperfusion period (0 to 24 h). Q-PCR was used to evaluate IFNα, IFNβ, IL-1β, IL-6 and TNF-α cytokine expression levels. Phosphorylation of signal transducers and activators of transcription (STAT)-1, STAT-3 and cleavage of caspase-3 was detected by western blot analysis. Post-OGD cellular viability was measured using a MTT assay.
resultsElevated IFNα and IFNβ expression was detected during reperfusion post-OGD in parental M17 cells. This correlated with enhanced phosphorylation of STAT-1, a downstream type-1 IFN signalling mediator. Significantly, ablation of type-1 IFN signalling, through IFNAR1 knockdown, reduced IFNα, IFNβ, IL-6 and TNF-α expression in response to OGD. In addition, MTT assay confirmed the IFNAR1 knockdown cells were protected against OGD compared to negative control cells with reduced pro-apoptotic cleaved caspase-3 levels.
conclusionsThis study confirms a role for type-1 IFN signalling in the neuro-inflammatory response following OGD in vitro and suggests its modulation through therapeutic blockade of IFNAR1 may be beneficial in reducing hypoxia-induced neuro-inflammation.
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