ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2016
Genetic ablation of soluble tumor necrosis factor with preservation of membrane tumor necrosis factor is associated with neuroprotection after focal cerebral ischemia.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 54 citations in OpenAlex.
- Single-cell analysis of microglia and monocyte dynamics uncovers distinct TNF-driven neuroimmune signatures in humans after intracerebral hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Single-Cell Analysis of Microglia and Monocyte Dynamics Uncover Distinct TNF-α-driven Neuroimmune Signatures after Intracerebral Hemorrhage.bioRxiv : the preprint server for biology · 2026Article
- The Role of TNF-α in Ischemic Stroke.International journal of molecular sciences · 2026Review
- The effect of the nonselective TNF inhibitor etanercept and of the selective TNF inhibitor XPro1595 on lesioned supraspinatus muscle.Bioscience reports · 2025Article
- Systemic inhibition of soluble TNF significantly changes glial cell populations leading to improved myelin integrity and better functional outcome after experimental stroke.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Microglial TNFR2 signaling regulates the inflammatory response after CNS injury in a sex-specific fashion.Brain, behavior, and immunity · 2024Article
- Noncanonical contribution of microglial transcription factor NR4A1 to post-stroke recovery through TNF mRNA destabilization.PLoS biology · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Tumor Necrosis Factor (TNF)-α-Stimulated Gene 6 (TSG-6): A Promising Immunomodulatory Target in Acute Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022Review
- Review
- Bibliometric analysis of tumor necrosis factor in post-stroke neuroinflammation from 2003 to 2021.Frontiers in immunology · 2022Article
- Dynamics of Microglia Activation in the Ischemic Brain: Implications for Myelin Repair and Functional Recovery.Frontiers in cellular neuroscience · 2022Review
- A wake-like state in vitro induced by transmembrane TNF/soluble TNF receptor reverse signaling.Brain, behavior, and immunity · 2021Article
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- Cytokines as therapeutic targets for cardio- and cerebrovascular diseases.Basic research in cardiology · 2021Review
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- Cooling and Sterile Inflammation in an Oxygen-Glucose-Deprivation/Reperfusion Injury Model in BV-2 Microglia.Mediators of inflammation · 2021Article
- Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
Microglia respond to focal cerebral ischemia by increasing their production of the neuromodulatory cytokine tumor necrosis factor, which exists both as membrane-anchored tumor necrosis factor and as cleaved soluble tumor necrosis factor forms. We previously demonstrated that tumor necrosis factor knockout mice display increased lesion volume after focal cerebral ischemia, suggesting that tumor necrosis factor is neuroprotective in experimental stroke. Here, we extend our studies to show that mice with intact membrane-anchored tumor necrosis factor, but no soluble tumor necrosis factor, display reduced infarct volumes at one and five days after stroke. This was associated with improved functional outcome after experimental stroke. No changes were found in the mRNA levels of tumor necrosis factor and tumor necrosis factor-related genes (TNFR1, TNFR2, TACE), pro-inflammatory cytokines (IL-1β, IL-6) or chemokines (CXCL1, CXCL10, CCL2); however, protein expression of TNF, IL-1β, IL-6 and CXCL1 was reduced in membrane-anchored tumor necrosis factor(Δ/Δ) compared to membrane-anchored tumor necrosis factor(wt/wt) mice one day after experimental stroke. This was paralleled by reduced MHCII expression and a reduction in macrophage infiltration in the ipsilateral cortex of membrane-anchored tumor necrosis factor(Δ/Δ) mice. Collectively, these findings indicate that membrane-anchored tumor necrosis factor mediates the protective effects of tumor necrosis factor signaling in experimental stroke, and therapeutic strategies specifically targeting soluble tumor necrosis factor could be beneficial in clinical stroke therapy.
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Registered trials
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