ArticleBiochimica et biophysica acta2014
Cold-inducible RNA-binding protein mediates neuroinflammation in cerebral ischemia.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
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Who cites it
67 citing papers in PubMed, 104 citations in OpenAlex.
- Targeting CIRP and IL-6R-mediated microglial inflammation to improve outcomes in intracerebral hemorrhage.Journal of advanced research · 2026Article
- Radiation-induced eCIRP Causes Alzheimer's Disease-like Neuronal Tau Phosphorylation.Molecular neurobiology · 2026Article
- Role of eCIRP in Mediating Post-ischemia Microglial Phagocytosis via TREM-2 Receptor: Insights from Porcine and Mouse Cellular Models.Molecular neurobiology · 2026Article
- The Role of Cold-Inducible RNA-Binding Protein (CIRP) in Neurological Disorders.Brain sciences · 2026Review
- Targeting of CIRP attenuates osteoarthritis progression via suppressing TLR4/NF‑κB/NLRP3 signaling axis.International journal of molecular medicine · 2026Article
- Ionizing radiation and Alzheimer's disease: epidemiology, mechanisms, and eCIRP-mediated tau pathology.Frontiers in immunology · 2026Review
- Extracellular Cold-Inducible RNA-Binding Protein: Progress from Discovery to Present.International journal of molecular sciences · 2025Review
- Therapeutic Hypothermia Increases the Expression of RNA-binding Protein Motif 3 and Attenuates Cognitive Deficits Following Cardiac Arrest in Rats.Neurochemical research · 2025Article
- Extracellular cold-inducible RNA-binding protein in CNS injury: molecular insights and therapeutic approaches.Journal of neuroinflammation · 2025Review
- Article
- Anti-DAMP therapies for acute inflammation.Frontiers in immunology · 2025Review
- Therapeutic modulation of protein RBM3 for ischemic stroke treatment.Frontiers in pharmacology · 2025Review
- Article
- Extracellular cold-inducible RNA-binding protein mediated neuroinflammation and neuronal apoptosis after traumatic brain injury.Burns & trauma · 2024Article
- Neuronal Responses to Ischemia: Scoping Review of Insights from Human-Derived In Vitro Models.Cellular and molecular neurobiology · 2023Article
- Extracellular CIRP Induces Calpain Activation in Neurons via PLC-IPMolecular neurobiology · 2023Article
- Exosome-derived CIRP: An amplifier of inflammatory diseases.Frontiers in immunology · 2023Review
- Serum CIRP increases the risk of acute kidney injury after cardiac surgery.Frontiers in medicine · 2023Article
- Serum cold-inducible RNA-binding protein (CIRP) levels as a prognostic indicator in patients with acute ischemic stroke.Frontiers in neurology · 2023Article
- Kurarinone alleviates hemin-induced neuroinflammation and microglia-mediated neurotoxicity by shifting microglial M1/M2 polarization via regulating the IGF1/PI3K/Akt signaling.The Kaohsiung journal of medical sciences · 2022Article
7 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 1 country.
Funding
Abstract
backgroundNeuroinflammation is a key cascade after cerebral ischemia. Excessive production of proinflammatory mediators in ischemia exacerbates brain injury. Cold-inducible RNA-binding protein (CIRP) is a newly discovered proinflammatory mediator that can be released into the circulation during hemorrhage or septic shock. Here, we examine the involvement of CIRP in brain injury during ischemic stroke.
methodsStroke was induced by middle cerebral artery occlusion (MCAO). In vitro hypoxia was conducted in a hypoxia chamber containing 1% oxygen. CIRP and tumor necrosis factor-α (TNF-α) levels were assessed by RT-PCR and Western blot analysis.
resultsCIRP is elevated along with an upregulation of TNF-α expression in mouse brain after MCAO. In CIRP-deficient mice, the brain infarct volume, induction of TNF-α, and activation of microglia are markedly reduced after MCAO. Using microglial BV2 cells, we demonstrate that hypoxia induces the expression, translocation, and release of CIRP, which is associated with an increase of TNF-α levels. Addition of recombinant murine (rm) CIRP directly induces TNF-α release from BV2 cells and such induction is inhibited by neutralizing antisera to CIRP. Moreover, rmCIRP activates the NF-κB signaling pathway in BV2 cells. The conditioned medium from BV2 cells exposed to hypoxia triggers the apoptotic cascade by increasing caspase activity and decreasing Bcl-2 expression in neural SH-SY5Y cells, which is inhibited by antisera to CIRP.
conclusionExtracellular CIRP is a detrimental factor in stimulating inflammation to cause neuronal damage in cerebral ischemia. GENERAL SIGNIFICANCE: Development of an anti-CIRP therapy may benefit patients with brain ischemia.
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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 Socratic graph.