ArticleJournal of cellular and molecular medicine2015
Poly (I:C) therapy decreases cerebral ischaemia/reperfusion injury via TLR3-mediated prevention of Fas/FADD interaction.
Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Pre- and post-conditioning with poly I:C exerts neuroprotective effect against cerebral ischemia injury in animal models: A systematic review and meta-analysis.CNS neuroscience & therapeutics · 2022Pooled it
- TLR3 activation in astrocytes attenuates the nigrostriatal pathway degeneration in rodent models of Parkinson's disease.Frontiers in cellular neuroscience · 2026Article
- Mechanisms and Clinical Significance of Endosomal Toll-Like Receptors in Neurological Diseases.Molecular neurobiology · 2025Review
- Exploring the mediating role of potential therapeutic genes in the pathogenesis of hypopituitarism through the metabolites from a genomic perspective.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- FAS-mediated circRNA-miRNA-mRNA Crosstalk Network Regulates Immune Cell Infiltration in Cerebral Infarction.Journal of molecular neuroscience : MN · 2023Article
- Perinatal exposure to synergistic multiple stressors leads to cellular and behavioral deficits mimicking Schizophrenia-like pathology.Biology open · 2022Article
- Viral mimetic triggers cerebral arteriopathy in juvenile brain via neutrophil elastase and NETosis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Cathepsin H deficiency decreases hypoxia-ischemia-induced hippocampal atrophy in neonatal mice through attenuated TLR3/IFN-β signaling.Journal of neuroinflammation · 2021Article
- Poly(I:C) preconditioning protects the heart against myocardial ischemia/reperfusion injury through TLR3/PI3K/Akt-dependent pathway.Signal transduction and targeted therapy · 2020Article
- RNA Signaling in Pulmonary Arterial Hypertension-A Double-Stranded Sword.International journal of molecular sciences · 2020Review
- The role of Toll-like receptor signaling pathways in cerebrovascular disorders: the impact of spreading depolarization.Journal of neuroinflammation · 2020Review
- Toll-like receptor 3 activation increases voluntary alcohol intake in C57BL/6J male mice.Brain, behavior, and immunity · 2019Article
- Potential Medications or Compounds Acting on Toll-like Receptors in Cerebral Ischemia.Current neuropharmacology · 2018Review
- The Role of Toll-Like Receptors and Vitamin D in Cardiovascular Diseases-A Review.International journal of molecular sciences · 2017Review
- Toward RNA nanoparticle vaccines: synergizing RNA and inorganic nanoparticles to achieve immunopotentiation.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2017Review
- Toll-like Receptors in the Vascular System: Sensing the Dangers Within.Pharmacological reviews · 2016Review
- Immunomodulatory Effect of Toll-Like Receptor-3 Ligand Poly I:C on Cortical Spreading Depression.Molecular neurobiology · 2016Article
- Function and mechanism of toll-like receptors in cerebral ischemic tolerance: from preconditioning to treatment.Journal of neuroinflammation · 2015Review
- Engagement of Fas on Macrophages Modulates Poly I:C induced cytokine production with specific enhancement of IP-10.PloS one · 2015Article
- Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Toll-like receptor (TLR)-mediated signalling plays a role in cerebral ischaemia/reperfusion (I/R) injury. Modulation of TLRs has been reported to protect against cerebral I/R injury. This study examined whether modulation of TLR3 with poly (I:C) will induce protection against cerebral I/R injury. Mice were treated with or without Poly (I:C) (n = 8/group) 1 hr prior to cerebral ischaemia (60 min.) followed by reperfusion (24 hrs). Poly (I:C) pre-treatment significantly reduced the infarct volume by 57.2% compared with untreated I/R mice. Therapeutic administration of Poly (I:C), administered 30 min. after cerebral ischaemia, markedly decreased infarct volume by 34.9%. However, Poly (I:C)-induced protection was lost in TLR3 knockout mice. In poly (I:C)-treated mice, there was less neuronal damage in the hippocampus compared with untreated I/R mice. Poly (I:C) treatment induced IRF3 phosphorylation, but it inhibited NF-κB activation in the brain. Poly (I:C) also decreased I/R-induced apoptosis by attenuation of Fas/FasL-mediated apoptotic signalling. In addition, Poly (I:C) treatment decreased microglial cell caspase-3 activity. In vitro data showed that Poly (I:C) prevented hypoxia/reoxygenation (H/R)-induced interaction between Fas and FADD as well as caspase-3 and -8 activation in microglial cells. Importantly, Poly (I:C) treatment induced co-association between TLR3 and Fas. Our data suggest that Poly (I:C) decreases in cerebral I/R injury via TLR3 which associates with Fas, thereby preventing the interaction of Fas and FADD, as well as microglial cell caspase-3 and -8 activities. We conclude that TLR3 modulation by Poly (I:C) could be a potential approach for protection against ischaemic stroke.
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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.