ArticleJournal of neurochemistry2014
Ischemic neurons activate astrocytes to disrupt endothelial barrier via increasing VEGF expression.
Article in Journal of neurochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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The trial behind it
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Who cites it
66 citing papers in PubMed, 117 citations in OpenAlex.
- The intersection of circadian rhythms and the blood-brain barrier with drug efficacy and delivery in neurological disorders.Advanced drug delivery reviews · 2025Review
- HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.Translational stroke research · 2025Review
- VEGF-E Attenuates Injury After Ischemic Stroke by Promoting Reparative Revascularization.The European journal of neuroscience · 2025Article
- The dual role of VEGF-A in a complex in vitro model of oxaliplatin-induced neurotoxicity: Pain-related and neuroprotective effects.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- The therapeutic effects and mechanisms of glucagon-like peptide-1 receptor agonists in neurocognitive disorders.Therapeutic advances in neurological disorders · 2025Review
- The Role of Gut Microbiota in Blood-Brain Barrier Disruption after Stroke.Molecular neurobiology · 2024Review
- Alzheimer's disease and drug delivery across the blood-brain barrier: approaches and challenges.European journal of medical research · 2024Review
- Astrocyte-Derived Extracellular Vesicles for Ischemic Stroke: Therapeutic Potential and Prospective.Aging and disease · 2024Review
- Clarifying the mechanism of apigenin against blood-brain barrier disruption in ischemic stroke using systems pharmacology.Molecular diversity · 2024Article
- Fluid biomarkers of the neurovascular unit in cerebrovascular disease and vascular cognitive disorders: A systematic review and meta-analysis.Cerebral circulation - cognition and behavior · 2024Article
- Role of Crosstalk between Glial Cells and Immune Cells in Blood-Brain Barrier Damage and Protection after Acute Ischemic Stroke.Aging and disease · 2023Review
- Pathophysiology and probable etiology of cerebral small vessel disease in vascular dementia and Alzheimer's disease.Molecular neurodegeneration · 2023Review
- A newly-synthesized compound CP-07 alleviates microglia-mediated neuroinflammation and ischemic brain injury via inhibiting STAT3 phosphorylation.Journal of translational internal medicine · 2023Article
- Physiological and pathological consequences of exosomes at the blood-brain-barrier interface.Cell communication and signaling : CCS · 2023Review
- Blood-Brain Barrier Integrity Damage in Bacterial Meningitis: The Underlying Link, Mechanisms, and Therapeutic Targets.International journal of molecular sciences · 2023Review
- The blood-brain barrier in health, neurological diseases, and COVID-19.Fundamental research · 2022Review
- Network Pharmacology Experiments Show That Emodin Can Exert a Protective Effect on MCAO Rats by Regulating Hif-1α/VEGF-A Signaling.ACS omega · 2022Article
- VEGF, a Key Factor for Blood Brain Barrier Injury After Cerebral Ischemic Stroke.Aging and disease · 2022Article
- Vascular derived endothelin receptor A controls endothelin-induced retinal ganglion cell death.Cell death discovery · 2022Article
- Hemorrhagic Transformation After Tissue Plasminogen Activator Treatment in Acute Ischemic Stroke.Cellular and molecular neurobiology · 2022Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Blood-brain barrier (BBB) disruption occurring within the first few hours of ischemic stroke onset is closely associated with hemorrhagic transformation following thrombolytic therapy. However, the mechanism of this acute BBB disruption remains unclear. In the neurovascular unit, neurons do not have direct contact with the endothelial barrier; however, they are highly sensitive and vulnerable to ischemic injury, and may act as the initiator for disrupting BBB when cerebral ischemia occurs. Herein, we employed oxygen-glucose deprivation (OGD) and an in vitro BBB system consisting of brain microvascular cells and astrocytes to test this hypothesis. Neurons (CATH.a cells) were exposed to OGD for 3-h before co-culturing with endothelial monolayer (bEnd 3 cells), or endothelial cells plus astrocytes (C8-D1A cells). Incubation of OGD-treated neurons with endothelial monolayer alone did not increase endothelial permeability. However, when astrocytes were present, the endothelial permeability was significantly increased, which was accompanied by loss of occludin and claudin-5 proteins as well as increased vascular endothelial growth factor (VEGF) secretion into the conditioned medium. Importantly, all these changes were abolished when VEGF was knocked down in astrocytes by siRNA. Our findings suggest that ischemic neurons activate astrocytes to increase VEGF production, which in turn induces endothelial barrier disruption.
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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.