ArticleThe European journal of neuroscience2025
VEGF-E Attenuates Injury After Ischemic Stroke by Promoting Reparative Revascularization.
Article in The European journal of neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Impact of Short-term Rehabilitation on Chronic Stress-induced Brain Alterations and Associated Cognitive Deficits.Annals of neurosciences · 2026Article
- Research on the mechanism of human umbilical cord mesenchymal stem cells and their extracellular vesicles in the treatment of common reproductive diseases.Stem cell research & therapy · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
The angiogenic response after stroke correlates with mild injury and an improved recovery. Stimulation of post-stroke angiogenesis using vascular endothelial growth factor (VEGF)-A is associated with an increased risk of vascular destabilization, leading to life-threatening complications. The non-mammalian VEGF-A homolog, VEGF-E, stimulates stable cutaneous vascularization and promotes wound healing. Herein, we posit that VEGF-E represents a potential mediator of reparative revascularization after ischemic stroke. C57BL6/J wildtype mice were subjected to experimental stroke, and VEGF-E or VEGF-A were intranasally delivered during the subacute phase. Our results indicate that VEGF-E improves neurological recovery and increases vascular density without compromising permeability, more efficiently than VEGF-A. We show that VEGF-E-mediated revascularization correlates with normal restoration of brain perfusion, whereas VEGF-A induces cerebral hyperperfusion, indicative of vascular dysfunction. Furthermore, VEGF-E reduces microvascular stalls, increases the density of angiogenic vasculature, and improves the interaction of brain endothelial cell with pericytes, which is critical for vascular stabilization. Using cell-based assays, we demonstrate that stimulation of brain endothelial cells with VEGF-E, but not with VEGF-A, increases the expression of platelet-derived growth factor (PDGF)-D, a potent ligand of PDGFRβ that plays critical roles in regulating the survival and functions of perivascular cells, including pericytes. These effects are associated with activation of extracellular signal-regulated kinase (ERK)1/2 and P38 mitogen-activated protein kinase (MAPK). Finally, we confirm that the secretome of VEGF-E-stimulated brain endothelial cells ameliorates pericyte migration required for vascular recruitment. Our study indicates that VEGF-E promotes a stable and functional revascularization after ischemic stroke, outlining its promises for therapeutic purposes.
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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 Socratic graph.