ArticleFrontiers in cellular neuroscience2017
Loss of IRF2BP2 in Microglia Increases Inflammation and Functional Deficits after Focal Ischemic Brain Injury.
Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 50 citations in OpenAlex.
- The role of interferon regulatory factors in atherosclerosis: from cell type-specific mechanisms to therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- A 3'UTR polymorphism disrupts IRF2BP2 autoregulation through an eIF4H translational enhancer.Frontiers in genetics · 2026Article
- Ischemic stroke altered the expression profiles of super enhancer RNAs in mouse brain in a sexually dimorphic manner.Experimental neurology · 2025Article
- Mechanisms of Action of Propofol in Modulating Microglial Activation in Ischemic Stroke.Molecules (Basel, Switzerland) · 2025Review
- Functional diversity of cardiac macrophages in health and disease.Nature reviews. Cardiology · 2025Review
- Advancing Ischemic Stroke Prognosis: Key Role of MiR-155 Non-Coding RNA.International journal of molecular sciences · 2025Review
- The immunology of stroke and dementia.Immunity · 2025Review
- Bioinformatics analysis of electroacupuncture treatment for ischemic stroke: exploring transcriptional regulatory mechanisms mediated by super-enhancers.Frontiers in neuroscience · 2025Article
- Malate initiates a proton-sensing pathway essential for pH regulation of inflammation.Signal transduction and targeted therapy · 2024Article
- miR‑155 promotes an inflammatory response in HaCaT cells via the IRF2BP2/KLF2/NF‑κB pathway in psoriasis.International journal of molecular medicine · 2024Article
- Agmatine-IRF2BP2 interaction induces M2 phenotype of microglia by increasing IRF2-KLF4 signaling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- OIP5-AS1 Inhibits Oxidative Stress and Inflammation in Ischemic Stroke Through miR-155-5p/IRF2BP2 Axis.Neurochemical research · 2023Article
- REPAC: analysis of alternative polyadenylation from RNA-sequencing data.Genome biology · 2023Article
- Interferon-β modulates microglial polarization to ameliorate delayed tPA-exacerbated brain injury in ischemic stroke.Frontiers in immunology · 2023Article
- Didymin Alleviates Cerebral Ischemia-Reperfusion Injury by Activating the PPAR Signaling Pathway.Yonsei medical journal · 2022Article
- Inference of age-associated transcription factor regulatory activity changes in single cells.Nature aging · 2022Article
- Whole-exome sequencing in a subject with fluctuating neuropsychiatric symptoms, immunoglobulin G1 deficiency, and subsequent development of Crohn's disease: a case report.Journal of medical case reports · 2022Article
- Savior Siblings Might Rescue Fetal Lethality But Not Adult Lymphoma in Irf2bp2-Null Mice.Frontiers in immunology · 2022Article
- Differential Retinal Protein Expression in Primary and Secondary Retinal Ganglion Cell Degeneration Identified by Integrated SWATH and Target-Based Proteomics.International journal of molecular sciences · 2021Article
- Transient deSUMOylation of IRF2BP proteins controls early transcription in EGFR signaling.EMBO reports · 2021Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic stroke causes neuronal cell death and triggers a cascade of inflammatory signals that contribute to secondary brain damage. Microglia, the brain-resident macrophages that remove dead neurons, play a critical role in the brain's response to ischemic injury. Our previous studies showed that IRF2 binding protein 2 (IRF2BP2) regulates peripheral macrophage polarization, limits their inflammatory response and reduces susceptibility to atherosclerosis. Here, we show that loss of IRF2BP2 in microglia leads to increased inflammatory cytokine expression in response to lipopolysaccharide challenge and impaired activation of anti-inflammatory markers in response to interleukin-4 (IL4) stimulation. Focal ischemic brain injury of the sensorimotor cortex induced by photothrombosis caused more severe functional deficits in mice with IRF2BP2 ablated in macrophages/microglia, associated with elevated expression of inflammatory cytokines in the brain. These mutant mice had larger infarctions 4 days after stroke associated with fewer anti-inflammatory M2 microglia/macrophages recruited to the peri-infarct area, suggesting an impaired clearance of injured tissues. Since IRF2BP2 modulates interferon signaling, and interferon beta (IFNβ) has been reported to be anti-inflammatory and reduce ischemic brain injury, we asked whether loss of IRF2BP2 in macrophages/microglia would affect the response to IFNβ in our stroke model. IFNβ suppressed inflammatory cytokine production of macrophages and reduced infarct volumes at 4 days after photothrombosis in wild type mice. The anti-inflammatory effect of IFNβ was lost in IRF2BP2-deficient macrophages and IFNβ failed to protect mice lacking IRF2BP2 in macrophages/microglia from ischemic injury. In summary, IRF2BP2 expression in macrophages/microglia is important to limit inflammation and stroke injury, in part by mediating the beneficial effect of IFNβ.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.