ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Ocular neovascularization caused by herpes simplex virus type 1 infection results from breakdown of binding between vascular endothelial growth factor A and its soluble receptor.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A Systematic Review of Tear Vascular Endothelial Growth Factor and External Eye Diseases.International journal of molecular sciences · 2024Pooled it
- Extracellular matrix proteoglycans lumican and biglycan promote innate immune signals and viral clearance in HSV-1 infections of mouse corneas.bioRxiv : the preprint server for biology · 2026Article
- Molecular Pathways Driving Corneal Neovascularization in Herpes Simplex Keratitis.Pathogens (Basel, Switzerland) · 2026Review
- Review
- Peripheral Choroid/RPE/Sclera as a Shared Pathogenic Hub: Multi-Tissue Transcriptomic Profiling Identifies Common Differentially Expressed Genes in Age-Related Macular Degeneration and Alzheimer's Disease.Molecular neurobiology · 2025Article
- Review
- The immunobiology of corneal HSV-1 infection and herpetic stromal keratitis.Clinical microbiology reviews · 2024Review
- Models of Herpes Simplex Virus Latency.Viruses · 2024Review
- Meeting the Challenge of Controlling Viral Immunopathology.International journal of molecular sciences · 2024Review
- The Host-Pathogen Interplay: A Tale of Two Stories within the Cornea and Posterior Segment.Microorganisms · 2023Review
- Role of IL-27 in HSV-1-Induced Herpetic Stromal Keratitis.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis.Pathogens (Basel, Switzerland) · 2023Review
- Tear Film MicroRNAs as Potential Biomarkers: A Review.International journal of molecular sciences · 2023Review
- Aspects of Antiviral Strategies Based on Different Phototherapy Approaches: Hit by the Light.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Inhibitory effects of luteolin on TLR3-mediated inflammation caused by TAK/NF-κB signaling in human corneal fibroblasts.International journal of ophthalmology · 2022Article
- Osteopontin contributes to virus resistance associated with type I IFN expression, activation of downstream ifn-inducible effector genes, and CCR2Frontiers in immunology · 2022Article
- Microglia shield the murine brain from damage mediated by the cytokines IL-6 and IFN-α.Frontiers in immunology · 2022Article
- Host Molecules That Promote Pathophysiology of Ocular Herpes.Frontiers in microbiology · 2022Review
- Deliver protein across bio-barriers via hexa-histidine metal assemblies for therapy: a case in corneal neovascularization model.Materials today. Bio · 2021Article
- Topical administration of the kappa opioid receptor agonist nalfurafine suppresses corneal neovascularization and inflammation.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The normal cornea is transparent, which is essential for normal vision, and although the angiogenic factor vascular endothelial growth factor A (VEGF-A) is present in the cornea, its angiogenic activity is impeded by being bound to a soluble form of the VEGF receptor-1 (sVR-1). This report investigates the effect on the balance between VEGF-A and sVR-1 that occurs after ocular infection with HSV, which causes prominent neovascularization, an essential step in the pathogenesis of the vision-impairing lesion, stromal keratitis. We demonstrate that HSV-1 infection causes increased production of VEGF-A but reduces sVR-1 levels, resulting in an imbalance of VEGF-A and sVR-1 levels in ocular tissues. Moreover, the sVR-1 protein made was degraded by the metalloproteinase (MMP) enzymes MMP-2, -7, and -9 produced by infiltrating inflammatory cells that were principally neutrophils. Inhibition of neutrophils, inhibition of sVR-1 breakdown with the MMP inhibitor marimastat, and the provision of exogenous recombinant sVR-1 protein all resulted in reduced angiogenesis. Our results make the novel observation that ocular neovascularization resulting from HSV infection involves a change in the balance between VEGF-A and its soluble inhibitory receptor. Future therapies aimed to increase the production and activity of sVR-1 protein could benefit the management of stromal keratitis, an important cause of human blindness.
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