ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
CXCL16 orchestrates adenosine A3 receptor and MCP-1/CCL2 activity to protect neurons from excitotoxic cell death in the CNS.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 69 citations in OpenAlex.
- Vitamin D supplementation and systemic inflammation in relapsing-remitting multiple sclerosis.Journal of neurology · 2015Trial
- Recombinant CXCL16 reduces brain injury by modulating microglial phenotype and attenuating apoptosis in acute ischemic stroke.Scientific reports · 2026Article
- Renal Ischemia-Reperfusion and Uremic Toxins Modulate the Aortic Adenosinergic Axis in Acute Kidney Injury.International journal of molecular sciences · 2026Article
- STAT4-dependent regulation of neuroinflammation in atherosclerosis.Physiological reports · 2026Article
- STAT4-dependent regulation of neuroinflammation in atherosclerosis.bioRxiv : the preprint server for biology · 2026Article
- Inflammatory, clinical and sociodemographic factors associated with depressive disorder during pregnancy in Brazilian women.Scientific reports · 2026Article
- Probiotics derived sodium benzoate improves social behavior of offspring exposed in the maternal immune activation through regulation of histone lysine benzoylation in astrocytes.Molecular psychiatry · 2025Article
- Genes That Associated with Action of ACTH-like Peptides with Neuroprotective Potential in Rat Brain Regions with Different Degrees of Ischemic Damage.International journal of molecular sciences · 2025Article
- Prenatal Alcohol Exposure Disrupts CXCL16 Expression in Rat Hippocampus: Temporal and Sex Differences.International journal of molecular sciences · 2025Article
- Cortical Stimulation-Based Transcriptome Shifts on Parkinson's Disease Animal Model.ASN neuro · 2025Article
- Involvement of CXCL10 rs4256246, CXCR4 rs2228014, CCR2 rs1799864 and CXCL16 rs2277680 in the Predisposition to Schizophrenia.Journal of molecular neuroscience : MN · 2024Article
- Antibiotics treatment promotes vasculogenesis in the brain of glioma-bearing mice.Cell death & disease · 2024Article
- SRF-deficient astrocytes provide neuroprotection in mouse models of excitotoxicity and neurodegeneration.eLife · 2024Article
- Spinal Cord Stimulation Increases Chemoefficacy and Prevents Paclitaxel-Induced Pain via CX3CL1.Neuromodulation : journal of the International Neuromodulation Society · 2023Article
- The impact of inosine on hippocampal synaptic transmission and plasticity involves the release of adenosine through equilibrative nucleoside transporters rather than the direct activation of adenosine receptors.Purinergic signalling · 2023Article
- A novel transgenic mouse model expressing primate-specific nuclear choline acetyltransferase: insights into potential cholinergic vulnerability.Scientific reports · 2023Article
- Remodeling of astrocyte secretome in amyotrophic lateral sclerosis: uncovering novel targets to combat astrocyte-mediated toxicity.Translational neurodegeneration · 2022Review
- Single-cell RNA transcriptome analysis of CNS immune cells reveals CXCL16/CXCR6 as maintenance factors for tissue-resident T cells that drive synapse elimination.Genome medicine · 2022Article
- Review
- Cellular, synaptic, and network effects of chemokines in the central nervous system and their implications to behavior.Pharmacological reports : PR · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A role for chemokines as molecules mediating neuron-glia cross talk has emerged in recent years, both in physiological and pathological conditions. We demonstrate here for the first time that the chemokine CXCL16 and its unique receptor CXCR6 are functionally expressed in the CNS, and induce neuroprotection against excitotoxic damage due to excessive glutamate (Glu) exposure and oxygen glucose deprivation (OGD). In mice and rats we found that, to exert neuroprotection, CXCL16 requires the presence of extracellular adenosine (ADO), and that pharmacological or genetic inactivation of the ADO A(3) receptor, A(3)R, prevents CXCL16 effect. In experiments with astrocytes cocultured with cxcr6(gfp/gfp) hippocampal cells, we demonstrate that CXCL16 acts directly on astrocytes to release soluble factors that are essential to mediate neuroprotection. In particular, we report that (1) upon stimulation with CXCL16 astrocytes release monocyte chemoattractant protein-1/CCL2 and (2) the neuroprotective effect of CXCL16 is reduced in the presence of neutralizing CCL2 antibody. In conclusion, we found that chemokine CXCL16 is able to mediate cross talk between astrocytes and neighboring neurons and, in pathological conditions such as excessive Glu or OGD exposure, is able to counteract neuronal cell death through an ADO-dependent chemokine-induced chemokine-release mechanism.
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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.