ArticleThe Journal of clinical investigation2016
Truncated netrin-1 contributes to pathological vascular permeability in diabetic retinopathy.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 52 citations in OpenAlex.
- Microglia-vascular interactions after spinal cord injury: regulatory mechanisms and therapeutic advances.Frontiers in immunology · 2026Review
- Nerve tissue model on a micropatterned surface: Axon guidance and neural regeneration.Journal of materials science. Materials in medicine · 2025Article
- Netrin-1 inhibits the attachment and internalization of Hepatitis B virus for hepatocyte infection.PLoS pathogens · 2025Article
- Restoring compromised blood-retina-barrier integrity with Netrin-1 overexpression.Cellular and molecular life sciences : CMLS · 2025Article
- Article
- Netrin-1 and RGMa: Novel Regulators of Atherosclerosis-Related Diseases.Cardiovascular drugs and therapy · 2025Review
- Netrin-1: Dual Roles in Neuroinflammation and Neurodegenerative Disease Dynamics.International journal of inflammation · 2025Review
- Interplay between Netrin-1 and Norrin controls arteriovenous zonation of blood-retina barrier integrity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Protein O-GlcNAcylation coupled to Hippo signaling drives vascular dysfunction in diabetic retinopathy.Nature communications · 2024Article
- Nanoparticle Targeting Strategies for Lipid and Polymer-Based Gene Delivery to Immune Cells In Vivo.Small science · 2024Article
- Single-cell transcriptomic analysis reveals the antiangiogenic role of Mgarp in diabetic retinopathy.BMJ open diabetes research & care · 2024Article
- Proteolytic regulation of a galectin-3/Lrp1 axis controls osteoclast-mediated bone resorption.The Journal of cell biology · 2023Article
- The dynamic nature of netrin-1 and the structural basis for glycosaminoglycan fragment-induced filament formation.Nature communications · 2023Article
- MicroRNA-based engineering of mesenchymal stem cell extracellular vesicles for treatment of retinal ischemic disorders: Engineered extracellular vesiclesand retinal ischemia.Acta biomaterialia · 2023Article
- A bone to pick-cellular and molecular mechanisms of bone pain in sickle cell disease.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Association of Netrin 1 with hsCRP in Subjects with Obesity and Recent Diagnosis of Type 2 Diabetes.Current issues in molecular biology · 2022Article
- Netrin-1 Secreted by Human Osteoarthritic Articular Chondrocytes Promotes AngiogenesisCartilage · 2022Article
- Netrin-1: A Modulator of Macrophage Driven Acute and Chronic Inflammation.International journal of molecular sciences · 2021Review
- Netrin-1 as a Multitarget Barrier Stabilizer in the Peripheral Nerve after Injury.International journal of molecular sciences · 2021Article
- Silencing Myeloid Netrin-1 Induces Inflammation Resolution and Plaque Regression.Circulation research · 2021Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Diabetic retinopathy (DR) is a major complication of diabetes and a leading cause of blindness in the working-age population. Impaired blood-retinal barrier function leads to macular edema that is closely associated with the deterioration of central vision. We previously demonstrated that the neuronal guidance cue netrin-1 activates a program of reparative angiogenesis in microglia within the ischemic retina. Here, we provide evidence in both vitreous humor of diabetic patients and in retina of a murine model of diabetes that netrin-1 is metabolized into a bioactive fragment corresponding to domains VI and V of the full-length molecule. In contrast to the protective effects of full-length netrin-1 on retinal microvasculature, the VI-V fragment promoted vascular permeability through the uncoordinated 5B (UNC5B) receptor. The collagenase matrix metalloprotease 9 (MMP-9), which is increased in patients with diabetic macular edema, was capable of cleaving netrin-1 into the VI-V fragment. Thus, MMP-9 may release netrin-1 fragments from the extracellular matrix and facilitate diffusion. Nonspecific inhibition of collagenases or selective inhibition of MMP-9 decreased pathological vascular permeability in a murine model of diabetic retinal edema. This study reveals that netrin-1 degradation products are capable of modulating vascular permeability, suggesting that these fragments are of potential therapeutic interest for the treatment of DR.
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