ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Interleukin-1alpha and HMGB1 mediate hippocampal dysfunction in SIGIRR-deficient mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 65 citations in OpenAlex.
- Landscape of copy number variants in Spanish people with dementia.NPJ genomic medicine · 2026Article
- IGF2BP2-Shox2 axis regulates hippocampal-neuronal senescence to alleviate microgravity-induced recognition disturbance.iScience · 2024Article
- Circulating HMGB1 in acute ischemic stroke and its association with post-stroke cognitive impairment.PeerJ · 2024Article
- A mechanistic review of pharmacological activities of homeopathic medicine licorice against neural diseases.Frontiers in neuroscience · 2023Review
- Prolonged Febrile Seizures Impair Synaptic Plasticity and Alter Developmental Pattern of Glial Fibrillary Acidic Protein (GFAP)-Immunoreactive Astrocytes in the Hippocampus of Young Rats.International journal of molecular sciences · 2022Article
- Palmitic Acid and Oleic Acid Differently Modulate TLR2-Mediated Inflammatory Responses in Microglia and Macrophages.Molecular neurobiology · 2022Article
- Research on the Mechanism of HMGB1 Regulating Autoimmune Encephalomyelitis by Regulating NF-Journal of healthcare engineering · 2022Article
- Negative Regulation of the IL-1 System by IL-1R2 and IL-1R8: Relevance in Pathophysiology and Disease.Frontiers in immunology · 2022Review
- HMGB1 mediates cognitive impairment caused by the NLRP3 inflammasome in the late stage of traumatic brain injury.Journal of neuroinflammation · 2021Article
- Inhibition of Urea Transporter (UT)-B Modulates LPS-Induced Inflammatory Responses in BV2 Microglia and N2a Neuroblastoma Cells.Neurochemical research · 2021Article
- Rosmarinic acid suppresses tau phosphorylation and cognitive decline by downregulating the JNK signaling pathway.NPJ science of food · 2021Article
- Hippocampal Function Is Impaired by a Short-Term High-Fat Diet in Mice: Increased Blood-Brain Barrier Permeability and Neuroinflammation as Triggering Events.Frontiers in neuroscience · 2021Article
- The Role of Neuroinflammation in Post-traumatic Epilepsy.Frontiers in neurology · 2021Review
- The deubiquitinase USP13 stabilizes the anti-inflammatory receptor IL-1R8/Sigirr to suppress lung inflammation.EBioMedicine · 2019Article
- Review
- Tuning inflammation and immunity by the negative regulators IL-1R2 and IL-1R8.Immunological reviews · 2018Review
- The Communication Between the Immune and Nervous Systems: The Role of IL-1β in Synaptopathies.Frontiers in molecular neuroscience · 2018Review
- Inhibition of IL-1β Signaling Normalizes NMDA-Dependent Neurotransmission and Reduces Seizure Susceptibility in a Mouse Model of Creutzfeldt-Jakob Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Article
- Pharmacological Tools to Activate Microglia and their Possible use to Study Neural Network Patho-physiology.Current neuropharmacology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Single-Ig-interleukin-1 related receptor (SIGIRR) is a member of the interleukin (IL)-1/Toll-like receptor (TLR) family. It negatively regulates inflammation, rendering SIGIRR(-/-) mice more susceptible to inflammatory challenge. This susceptibility extends to the brain, where increased responsiveness to lipopolysaccharide has been observed in SIGIRR-deficient mice. While this is likely due to enhanced TLR4-mediated signaling, the functional consequences of these changes have not yet been described. In the current study, we have investigated the impact of SIGIRR deficiency on hippocampal function, and show that novel object recognition, spatial reference memory, and long-term potentiation (LTP) were impaired in SIGIRR(-/-) mice. These changes were accompanied by increased expression of IL-1RI and TLR4, and upregulation of their downstream signaling events, namely IRAK1 (IL-1R-associated kinase 1), c-Jun N-terminal protein kinase (JNK), and nuclear factor κB (NF-κB). The deficit in LTP was attenuated by the endogenous IL-1 receptor antagonist (IL-1ra) and an anti-TLR4 antibody, and also by inhibition of JNK and NF-κB. We propose that IL-1RI is activated by IL-1α and TLR4 is activated by the endogenous agonist, high mobility group box 1 (HMGB1), as we identified enhanced expression of both cytokines in the hippocampus of SIGIRR(-/-) mice. Additionally, application of HMGB1 increased the activation of JNK and NF-κB and was found to be detrimental to LTP in a TLR4-dependent manner. These findings highlight the functional role of SIGIRR in regulating inflammatory-mediated synaptic and cognitive decline, and describe evidence of the key role of HMGB1 in this process.
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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.