ArticlePloS one2013
Evidence that the EphA2 receptor exacerbates ischemic brain injury.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- Profiling of hypoxic and extracellular matrix remodeling markers in biofluids and cerebral tissue after traumatic brain injury: expression and signaling crosstalk of HIF-1α, MMP-9/14 and EPHA2.International journal of legal medicine · 2026Article
- miR-302a-3p mitigates intervertebral disc degeneration progression through regulating EPHA2.Journal of orthopaedic surgery and research · 2025Article
- Dcaf15-mediated EphA2 degradation triggers disruption of the blood-brain barrier during Streptococcus suis meningitis.Communications biology · 2025Article
- Macropinocytosis mediates neurotropism ofResearch square · 2025Article
- Plasma circulating extracellular vesicles reveal dysregulation of synaptic signaling in SHIV-infected rhesus macaque.Cell communication and signaling : CCS · 2025Article
- Association among circulating erythropoietin-producing hepatoma A2, progranulin, and kidney function in individuals with diabetes.Journal of diabetes investigation · 2025Article
- Metabolic and Inflammatory Stimuli Impact Vascular Circulation and Cell Proliferation Processes in the Amygdala.Genes, brain, and behavior · 2025Article
- Selective neuronal expression of progranulin is sufficient to provide neuroprotective and anti-inflammatory effects after traumatic brain injury.Journal of neuroinflammation · 2024Article
- Endothelial deletion of EPH receptor A4 alters single-cell profile and Tie2/Akap12 signaling to preserve blood-brain barrier integrity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Role of Progranulin (PGRN) in the Pathogenesis of Ischemic Stroke.Cellular and molecular neurobiology · 2023Review
- Regorafenib inhibits EphA2 phosphorylation and leads to liver damage via the ERK/MDM2/p53 axis.Nature communications · 2023Article
- Polyphenols for the Treatment of Ischemic Stroke: New Applications and Insights.Molecules (Basel, Switzerland) · 2022Review
- Vascular Sema3E-Plexin-D1 Signaling Reactivation Promotes Post-stroke Recovery through VEGF Downregulation in Mice.Translational stroke research · 2022Article
- Insights on the Functional Role of Beta-Glucans in Fungal Immunity Using Receptor-Deficient Mouse Models.International journal of molecular sciences · 2021Review
- EphA2 overexpression reduces H2O2-induced damage of lens epithelial cells.Genetics and molecular biology · 2021Article
- Ephrin-Eph Signaling as a Novel Neuroprotection Path in Ischemic Stroke.Journal of molecular neuroscience : MN · 2020Review
- EphrinA1-Fc Attenuates Ventricular Remodeling and Dysfunction in Chronically Nonreperfused WT but not EphA2-R-M mice.International journal of molecular sciences · 2020Article
- Approaches to Manipulate Ephrin-A:EphA Forward Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2020Review
- EphA2 contributes to disruption of the blood-brain barrier in cerebral malaria.PLoS pathogens · 2020Article
- Direct myosin-2 inhibition enhances cerebral perfusion resulting in functional improvement after ischemic stroke.Theranostics · 2020Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ephrin (Eph) signaling within the central nervous system is known to modulate axon guidance, synaptic plasticity, and to promote long-term potentiation. We investigated the potential involvement of EphA2 receptors in ischemic stroke-induced brain inflammation in a mouse model of focal stroke. Cerebral ischemia was induced in male C57Bl6/J wild-type (WT) and EphA2-deficient (EphA2(-/-)) mice by middle cerebral artery occlusion (MCAO; 60 min), followed by reperfusion (24 or 72 h). Brain infarction was measured using triphenyltetrazolium chloride staining. Neurological deficit scores and brain infarct volumes were significantly less in EphA2(-/-) mice compared with WT controls. This protection by EphA2 deletion was associated with a comparative decrease in brain edema, blood-brain barrier damage, MMP-9 expression and leukocyte infiltration, and higher expression levels of the tight junction protein, zona occludens-1. Moreover, EphA2(-/-) brains had significantly lower levels of the pro-apoptotic proteins, cleaved caspase-3 and BAX, and higher levels of the anti-apoptotic protein, Bcl-2 as compared to WT group. We confirmed that isolated WT cortical neurons express the EphA2 receptor and its ligands (ephrin-A1-A3). Furthermore, expression of all four proteins was increased in WT primary cortical neurons following 24 h of glucose deprivation, and in the brains of WT mice following stroke. Glucose deprivation induced less cell death in primary neurons from EphA2(-/-) compared with WT mice. In conclusion, our data provide the first evidence that the EphA2 receptor directly contributes to blood-brain barrier damage and neuronal death following ischemic stroke.
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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.