ArticleJournal of the American Heart Association2014
The TLR9 ligand, CpG-ODN, induces protection against cerebral ischemia/reperfusion injury via activation of PI3K/Akt signaling.
Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 64 citations in OpenAlex.
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- Exploring the Protective Effect and Potential Mechanism of Acutumidine on Myocardial Ischemia based on "Compound-Target-Pathway" Network.Combinatorial chemistry & high throughput screening · 2026Article
- Indobufen alleviates apoptosis by the PI3K/Akt/eNOS pathway in myocardial ischemia‒reperfusion (I/R) injury.Scientific reports · 2025Article
- Astrocyte-derived CXCL10 exacerbates endothelial cells pyroptosis and blood-brain barrier disruption via CXCR3/cGAS/AIM2 pathway after intracerebral hemorrhage.Cell death discovery · 2025Article
- Regulation of TAR DNA binding protein 43 (TDP-43) homeostasis by cytosolic DNA accumulation.The Journal of biological chemistry · 2024Article
- Inhibition of cGAS-STING pathway alleviates neuroinflammation-induced retinal ganglion cell death after ischemia/reperfusion injury.Cell death & disease · 2023Article
- Short-term toll-like receptor 9 inhibition leads to left ventricular wall thinning after myocardial infarction.ESC heart failure · 2023Article
- Neutrophil extracellular traps aggravate neuronal endoplasmic reticulum stress and apoptosis via TLR9 after traumatic brain injury.Cell death & disease · 2023Article
- The role of circulating cell-free DNA as an inflammatory mediator after stroke.Seminars in immunopathology · 2023Review
- Cytosine-phosphate-guanine oligodeoxynucleotides regulate the cell cycle, apoptosis, and steroidogenesis of mouse ovarian granulosa cells by targeting inhibin alpha (1 ~ 32) fragments.In vitro cellular & developmental biology. Animal · 2022Article
- Pathogenetic Mechanisms of Hypertension-Brain-Induced Complications: Focus on Molecular Mediators.International journal of molecular sciences · 2022Review
- Toll-Like Receptor Signaling Pathways: Novel Therapeutic Targets for Cerebrovascular Disorders.International journal of molecular sciences · 2021Review
- Pellino1 Contributes to Morphine Tolerance by Microglia Activation via MAPK Signaling in the Spinal Cord of Mice.Cellular and molecular neurobiology · 2020Article
- Selective nanoparticle-mediated targeting of renal tubular Toll-like receptor 9 attenuates ischemic acute kidney injury.Kidney international · 2020Article
- Inhibition of double-strand DNA-sensing cGAS ameliorates brain injury after ischemic stroke.EMBO molecular medicine · 2020Article
- The role of Toll-like receptor signaling pathways in cerebrovascular disorders: the impact of spreading depolarization.Journal of neuroinflammation · 2020Review
- The Trinity of cGAS, TLR9, and ALRs Guardians of the Cellular Galaxy Against Host-Derived Self-DNA.Frontiers in immunology · 2020Review
- CpG Oligonucleotides Protect Mice From Alphavirus Encephalitis: Role of NK Cells, Interferons, and TNF.Frontiers in immunology · 2020Article
- CpG-Oligodeoxynucleotides Alleviate Tert-Butyl Hydroperoxide-Induced Macrophage Apoptosis by Regulating Mitochondrial Function and Suppressing ROS Production.Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundToll-like receptors (TLRs) have been shown to be involved in cerebral ischemia/reperfusion (I/R) injury. TLR9 is located in intracellular compartments and recognizes CpG-DNA. This study examined the effect of CpG-ODN on cerebral I/R injury. METHODS AND
resultsC57BL/6 mice were treated with CpG-ODN by i.p. injection 1 hour before the mice were subjected to cerebral ischemia (60 minutes) followed by reperfusion (24 hours). Scrambled-ODN served as control-ODN. Untreated mice, subjected to cerebral I/R, served as I/R control. The effect of inhibitory CpG-ODN (iCpG-ODN) on cerebral I/R injury was also examined. In addition, we examined the therapeutic effect of CpG-ODN on cerebral I/R injury by administration of CpG-ODN 15 minutes after cerebral ischemia. CpG-ODN administration significantly decreased cerebral I/R-induced infarct volume by 69.7% (6.4±1.80% vs 21.0±2.85%, P<0.05), improved neurological scores, and increased survival rate, when compared with the untreated I/R group. Therapeutic administration of CpG-ODN also significantly reduced infarct volume by 44.7% (12.6±2.03% vs 22.8±2.54%, P<0.05) compared with untreated I/R mice. Neither control-ODN, nor iCpG-ODN altered I/R-induced cerebral injury or neurological deficits. Nissl staining showed that CpG-ODN treatment preserved neuronal morphology in the ischemic hippocampus. Immunoblot showed that CpG-ODN administration increased Bcl-2 levels by 41% and attenuated I/R-increased levels of Bax and caspase-3 activity in ischemic brain tissues. Importantly, CpG-ODN treatment induced Akt and GSK-3β phosphorylation in brain tissue and cultured microglial cells. PI3K inhibition with LY294002 abolished CpG-ODN-induced protection.
conclusionCpG-ODN significantly reduces cerebral I/R injury via a PI3K/Akt-dependent mechanism. Our data also indicate that CpG-ODN may be useful in the therapy of cerebral I/R injury.
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