ArticleFrontiers in neuroscience2019
Topical Administration of a Soluble TNF Inhibitor Reduces Infarct Volume After Focal Cerebral Ischemia in Mice.
Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- 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
- TNF as a mediator of metabolic inflammation and body-brain interaction in obesity-driven neuroinflammation and neurodegeneration.Ageing research reviews · 2025Review
- Bridging Inflammation and Repair: The Promise of MFG-E8 in Ischemic Stroke Therapy.International journal of molecular sciences · 2025Review
- 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
- Integrated single cell-RNA sequencing and Mendelian randomization for ischemic stroke and metabolic syndrome.iScience · 2024Article
- Naïve Inflammatory Proteome Profiles of Glucocorticoid Responsive Polymyalgia Rheumatica and Rheumatic Arthritis Patients-Links to Triggers and Proteomic Manifestations.Journal of personalized medicine · 2024Article
- Microglial TNFR2 signaling regulates the inflammatory response after CNS injury in a sex-specific fashion.Brain, behavior, and immunity · 2024Article
- Cuproptosis-related genes are involved in immunodeficiency following ischemic stroke.Archives of medical science : AMS · 2024Article
- Article
- Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS.Journal of neuroinflammation · 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
- Blood inflammatory markers and mortality in the US population: A Health and Retirement Survey (HRS) analysis.PloS one · 2023Article
- A preclinical randomized controlled multi-centre trial of anti-interleukin-17A treatment for acute ischaemic stroke.Brain communications · 2023Article
- Peripherally derived myeloid cells induce disease-dependent phenotypic changes in microglia.Frontiers in cellular neuroscience · 2023Article
- Bibliometric analysis of tumor necrosis factor in post-stroke neuroinflammation from 2003 to 2021.Frontiers in immunology · 2022Article
- Selective inhibition of soluble tumor necrosis factor signaling reduces abdominal aortic aneurysm progression.Frontiers in cardiovascular medicine · 2022Article
- A wake-like state in vitro induced by transmembrane TNF/soluble TNF receptor reverse signaling.Brain, behavior, and immunity · 2021Article
- Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundTumor necrosis factor, which exists both as a soluble (solTNF) and a transmembrane (tmTNF) protein, plays an important role in post-stroke inflammation. The objective of the present study was to test the effect of topical versus intracerebroventricular administration of XPro1595 (a solTNF inhibitor) and etanercept (a solTNF and tmTNF inhibitor) compared to saline on output measures such as infarct volume and post-stroke inflammation in mice.
methodsAdult male C57BL/6 mice were treated topically (2.5 mg/ml/1μl/h for 3 consecutive days) or intracerebroventricularly (1.25 mg/kg/0.5 ml, once) with saline, XPro1595, or etanercept immediately after permanent middle cerebral artery occlusion (pMCAO). Mice were allowed to survive 1 or 3 days. Infarct volume, microglial and leukocyte profiles, and inflammatory markers were evaluated.
resultsWe found that topical, and not intracerebroventricular, administration of XPro1595 reduced infarct volume at both 1 and 3 days after pMCAO. Etanercept showed no effect. We observed no changes in microglial or leukocyte populations. XPro1595 increased gene expression of
conclusionOur data demonstrate that topical administration of XPro1595 for 3 consecutive days decreases infarct volumes after ischemic stroke, while modifying microglial activation and the inflammatory response post-stroke. This suggests that inhibitors of solTNF hold great promise for future neuroprotective treatment in ischemic stroke.
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