ArticleJournal of neuroinflammation2024
Neuroinflammatory responses and blood-brain barrier injury in chronic alcohol exposure: role of purinergic P2 × 7 Receptor signaling.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- A neuroimmune framework for understanding adolescent stress and risk of alcohol misuse.Brain, behavior, & immunity - health · 2026Review
- miR-146a-5p mitigates ethanol-induced neuroinflammation by targeting Btg2-dependent microglial activation.Malawi medical journal : the journal of Medical Association of Malawi · 2026Article
- The P2X4-P2X7 purinergic axis in alcohol-related liver disease: from fibrogenesis to immunotherapy resistance.Purinergic signalling · 2026Review
- Microglial Plasticity in Vascular Dementia: Mechanisms and Therapeutic Reprogramming.International journal of molecular sciences · 2026Review
- P2X7R Signaling and Differential Regulation of Neuroinflammatory and Behavior Responses in Male and Female Mice During Chronic Ethanol Exposure.International journal of molecular sciences · 2026Article
- The effects of alcohol dependence on the CSF proteome in mice: Evidence for blood-brain barrier dysfunction and neuroinflammation.Neurobiology of disease · 2026Article
- Ethanol exposure and high-fat diet: assessing the neuroimmune and metabolic mechanisms in Alzheimer's disease pathology.Frontiers in neuroscience · 2026Review
- Molecular and biochemical correlates of frontal lobe white matter degeneration in humans with alcohol use disorder.Advances in drug and alcohol research · 2026Article
- Neutrophil Elastase (ELANE) as a Novel Neuroinflammatory Biomarker in Alcohol Use Disorder: Clinical Validation.Addiction biology · 2025Article
- The effects of Alcohol Dependence on the CSF Proteome in Mice: Evidence for Blood-Brain Barrier Dysfunction and Neuroinflammation.bioRxiv : the preprint server for biology · 2025Article
- Alcohol, aging, and the gut microbiome: Intersections of immunity, barrier dysfunction, and disease.Alcohol (Fayetteville, N.Y.) · 2025Review
- Purinergic and extracellular vesicle signaling in alcohol-induced blood-brain barrier breakdown and neuroimmune activation.Brain, behavior, and immunity · 2025Review
- Exploring the Causal Effect of Mitochondrial DNA Copy Number on Obstructive Sleep Apnea.Brain and behavior · 2025Article
- Binge alcohol and the neuroendocrinology of the aging female.Frontiers in neuroendocrinology · 2025Review
- Modulation of TNFα-driven neuroinflammation by Gardenin A: insights fromFrontiers in pharmacology · 2025Article
- Intracranial hemorrhage prediction in acute ischemic stroke patients with anterior circulation tandem lesions following endovascular thrombectomy.Frontiers in neurology · 2025Article
- Cell-free mitochondrial DNA as a pro-inflammatory agent in blood circulation: mechanisms, therapeutic implications, and clinical challenges in immune dysregulation.Frontiers in immunology · 2025Review
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Abstract
Alcohol consumption leads to neuroinflammation and blood‒brain barrier (BBB) damage, resulting in neurological impairment. We previously demonstrated that ethanol-induced disruption of barrier function in human brain endothelial cells was associated with mitochondrial injury, increased ATP and extracellular vesicle (EV) release, and purinergic receptor P2 × 7R activation. Therefore, we aimed to evaluate the effect of P2 × 7R blockade on peripheral and neuro-inflammation in ethanol-exposed mice. In a chronic intermittent ethanol (CIE)-exposed mouse model, P2 × 7R was inhibited by two different methods: Brilliant Blue G (BBG) or gene knockout. We assessed blood ethanol concentration (BEC), brain microvessel gene expression by using RT2 PCR array, plasma P2 × 7R and P-gp, serum ATP, EV-ATP, number of EVs, and EV mtDNA copy numbers. An RT2 PCR array of brain microvessels revealed significant upregulation of proinflammatory genes involved in apoptosis, vasodilation, and platelet activation in CIE-exposed wild-type animals, which were decreased 15-50-fold in BBG-treated-CIE-exposed animals. Plasma P-gp levels and serum P2 × 7R shedding were significantly increased in CIE-exposed animals. Pharmacological or genetic suppression of P2 × 7R decreased receptor shedding to levels equivalent to those in control group. The increase in EV number and EV-ATP content in the CIE-exposed mice was significantly reduced by P2 × 7R inhibition. CIE mice showed augmented EV-mtDNA copy numbers which were reduced in EVs after P2 × 7R inhibition or receptor knockout. These observations suggested that P2 × 7R signaling plays a critical role in ethanol-induced brain injury. Increased extracellular ATP, EV-ATP, EV numbers, and EV-mtDNA copy numbers highlight a new mechanism of brain injury during alcohol exposure via P2 × 7R and biomarkers of such damage. In this study, for the first time, we report the in vivo involvement of P2 × 7R signaling in CIE-induced brain injury.
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