ArticleNeuroscience2014
Interleukin-1β enhances neuronal vulnerability to proNGF-mediated apoptosis by increasing surface expression of p75(NTR) and sortillin.
Article in Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 37 citations in OpenAlex.
- Caloric restriction attenuates oxidative and inflammatory markers of aging, while compromising germinative epithelium homeostasis in the rat aged testis.Journal of endocrinological investigation · 2026Article
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- Sortilin is dispensable for secondary injury processes following traumatic brain injury in mice.Heliyon · 2024Article
- SARS-CoV-2 envelope protein triggers depression-like behaviors and dysosmia via TLR2-mediated neuroinflammation in mice.Journal of neuroinflammation · 2023Article
- Etiological Roles of p75Cells · 2023Article
- Inflammatory cytokines TNFα, IL-1β, and IL-6 are induced in endotoxin- stimulated microglia through different signaling cascades.Science progress · 2021Article
- Dexmedetomidine Alleviates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting p75NTR-Mediated Oxidative Stress and Apoptosis.Oxidative medicine and cellular longevity · 2020Article
- Nerve Growth Factor and Pathogenesis of Leprosy: Review and Update.Frontiers in immunology · 2018Review
- Microglia and CNS Interleukin-1: Beyond Immunological Concepts.Frontiers in neurology · 2018Review
- Fibroblast growth factor 22 is a novel modulator of depression through interleukin-1β.CNS neuroscience & therapeutics · 2017Article
- Chemokine CCL2-CCR2 Signaling Induces Neuronal Cell Death via STAT3 Activation and IL-1β Production after Status Epilepticus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- A novel antagonist of p75NTR reduces peripheral expansion and CNS trafficking of pro-inflammatory monocytes and spares function after traumatic brain injury.Journal of neuroinflammation · 2016Article
- A role for the p75 neurotrophin receptor in axonal degeneration and apoptosis induced by oxidative stress.The Journal of biological chemistry · 2014Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Many types of injury such as seizure, ischemia, and oxidative stress cause upregulation of the p75 neurotrophin receptor (p75(NTR)) in brain neurons, where it promotes apoptosis, however the mechanism by which p75(NTR) is regulated under these conditions is not well understood. Proinflammatory cytokines such as interleukin-1β (IL-1β) are highly produced under these injury conditions and, in particular, are expressed rapidly in the rat hippocampus after seizure. IL-1β is known to increase neuronal vulnerability under many conditions, although it does not directly induce neuronal death. Recently, we have shown that these cytokines regulate p75(NTR) induction both in neurons and astrocytes in vitro. Here, we show that IL-1β infusion into the brain induces p75(NTR) in neurons of the CA1 area of the hippocampus. While IL-1β induction of p75(NTR) is not sufficient to induce cell death, we demonstrate that IL-1β primes the neurons by recruiting p75(NTR) and its coreceptor sortilin to the cell surface, making the neurons more vulnerable to subsequent challenge by proNGF. These results suggest a mechanism by which IL-1β exacerbates neuronal death following injury.
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Registered trials
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.