ArticleJournal of neuroinflammation2011
Interleukin-1α expression precedes IL-1β after ischemic brain injury and is localised to areas of focal neuronal loss and penumbral tissues.
Article in Journal of neuroinflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 137 citations in OpenAlex.
- Article
- The Dynamics of Neuroinflammation in Traumatic Brain Injury: Molecular Markers Useful for Establishing the Post-Traumatic Interval in Forensic Practice.International journal of molecular sciences · 2026Review
- Brain-infiltrating CD8 T cells retain functional activity to protect against acute Zika virus infection.Scientific reports · 2026Article
- Characterizing inflammatory biomarkers in post-stroke seizure risk and outcome prognostication.PloS one · 2026Article
- Article
- IL-1 family cytokines in inflammation and immunity.Cellular & molecular immunology · 2025Review
- Chronic Ketosis Provides Neuroprotection Through HIF- 1α-Mediated Control of the TXNIP/NLRP3 Axis by Regulating the Inflammatory and Apoptotic Response.Molecular neurobiology · 2025Article
- Emodin influences pyroptosis-related Caspase 1-GSDMD axis alleviated cerebral ischemia-reperfusion injury in rats.Scientific reports · 2025Article
- Review
- Gene Expression Profile of Cultured Human Coronary Arterial Endothelial Cells Exposed to Serum from Chronic Kidney Disease Patients: Role ofInternational journal of molecular sciences · 2025Article
- Astrocytes in aging.Neuron · 2025Review
- Global Deficiency of Alzheimer's Disease Risk GeneASN neuro · 2025Article
- Expanding Role of Interleukin-1 Family Cytokines in Acute Ischemic Stroke.International journal of molecular sciences · 2024Review
- Hemorrhagic Shock and Resuscitation Causes Excessive Dopaminergic Signaling in the mPFC and Cognitive Dysfunction.Molecular neurobiology · 2024Article
- Molecular Pathogenesis of Ischemic and Hemorrhagic Strokes: Background and Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Interleukins in Epilepsy: Friend or Foe.Neuroscience bulletin · 2024Review
- Deciphering Post-Stroke Sleep Disorders: Unveiling Neurological Mechanisms in the Realm of Brain Science.Brain sciences · 2024Review
- CDR1as regulates α-synuclein-mediated ischemic brain damage by controlling miR-7 availability.Molecular therapy. Nucleic acids · 2023Article
- Stroke: Molecular mechanisms and therapies: Update on recent developments.Neurochemistry international · 2023Review
- Neutrophil Heterogeneity and its Roles in the Inflammatory Network after Ischemic Stroke.Current neuropharmacology · 2023Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundCerebral ischemia is a devastating condition in which the outcome is heavily influenced by inflammatory processes, which can augment primary injury caused by reduced blood supply. The cytokines interleukin-1α (IL-1α) and IL-1β are key contributors to ischemic brain injury. However, there is very little evidence that IL-1 expression occurs at the protein level early enough (within hours) to influence brain damage after stroke. In order to determine this we investigated the temporal and spatial profiles of IL-1α and IL-1β expression after cerebral ischemia.
findingsWe report here that in mice, as early as 4 h after reperfusion following ischemia induced by occlusion of the middle cerebral artery, IL-1α, but not IL-1β, is expressed by microglia-like cells in the ischemic hemisphere, which parallels an upregulation of IL-1α mRNA. 24 h after ischemia IL-1α expression is closely associated with areas of focal blood brain barrier breakdown and neuronal death, mostly near the penumbra surrounding the infarct. The sub-cellular distribution of IL-1α in injured areas is not uniform suggesting that it is regulated.
conclusionsThe early expression of IL-1α in areas of focal neuronal injury suggests that it is the major form of IL-1 contributing to inflammation early after cerebral ischemia. This adds to the growing body of evidence that IL-1α is a key mediator of the sterile inflammatory response.
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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.