ArticleScience signaling2015
SOCS3 in retinal neurons and glial cells suppresses VEGF signaling to prevent pathological neovascular growth.
Article in Science signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The trial behind it
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Identification of Biomarker in Kidney Stone Disease by Integrating Transcriptomics and Olink Proteomics: A Case-Control Study.Journal of inflammation research · 2026Article
- Crosstalk Between Neuronal and Glial Cells in Diabetic Retinopathy: Mechanisms and Implications for Neurodegeneration.Molecular neurobiology · 2025Review
- Modulation of microglial phagocytosis via the GAS6-MERTK pathway regulates pathological angiogenesis in the mouse oxygen-induced retinopathy model.Cell death & disease · 2025Article
- Botulinum neurotoxin serotype A inhibited ocular angiogenesis through modulating glial activation via SOCS3.Angiogenesis · 2024Article
- SOCS3 regulates pathological retinal angiogenesis through modulating SPP1 expression in microglia and macrophages.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Corneal application of SOCS1/3 peptides for the treatment of eye diseases mediated by inflammation and oxidative stress.Frontiers in immunology · 2024Review
- FAM222A, Part of the BET-Regulated Basal Endothelial Transcriptome, Is a Novel Determinant of Endothelial Biology and Angiogenesis-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Modulation of recovery from neonatal hyperoxic lung injury by sex as a biological variable.Redox biology · 2023Article
- Ocular Vascular Diseases: From Retinal Immune Privilege to Inflammation.International journal of molecular sciences · 2023Review
- Systemic Cytokines in Retinopathy of Prematurity.Journal of personalized medicine · 2023Review
- Suppressor of cytokine signaling 3-derived peptide as a therapeutic for inflammatory and oxidative stress-induced damage to the retina.Molecular vision · 2023Article
- Article
- Neurovascular abnormalities in retinopathy of prematurity and emerging therapies.Journal of molecular medicine (Berlin, Germany) · 2022Review
- TTI-101: A competitive inhibitor of STAT3 that spares oxidative phosphorylation and reverses mechanical allodynia in mouse models of neuropathic pain.Biochemical pharmacology · 2021Article
- Translational Research in Retinopathy of Prematurity: From Bedside to Bench and Back Again.Journal of clinical medicine · 2021Review
- SOCS3 Expression by Thymic Stromal Cells Is Required for Normal T Cell Development.Frontiers in immunology · 2021Article
- Targeting Neurovascular Interaction in Retinal Disorders.International journal of molecular sciences · 2020Review
- Targeting Neuroinflammation in Neovascular Retinal Diseases.Frontiers in pharmacology · 2020Review
- Protective effects of essential oil from FructusChinese medicine · 2020Article
- Maternal High-Fat Diet Consumption and Chronic Hyperandrogenemia Are Associated With Placental Dysfunction in Female Rhesus Macaques.Endocrinology · 2019Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Neurons and glial cells in the retina contribute to neovascularization, or the formation of abnormal new blood vessels, in proliferative retinopathy, a condition that can lead to vision loss or blindness. We identified a mechanism by which suppressor of cytokine signaling 3 (SOCS3) in neurons and glial cells prevents neovascularization. We found that Socs3 expression was increased in the retinal ganglion cell and inner nuclear layers after oxygen-induced retinopathy. Mice with Socs3 deficiency in neuronal and glial cells had substantially reduced vaso-obliterated retinal areas and increased pathological retinal neovascularization in response to oxygen-induced retinopathy, suggesting that loss of neuronal/glial SOCS3 increased both retinal vascular regrowth and pathological neovascularization. Furthermore, retinal expression of Vegfa (which encodes vascular endothelial growth factor A) was higher in these mice than in Socs3 flox/flox controls, indicating that neuronal and glial SOCS3 suppressed Vegfa expression during pathological conditions. Lack of neuronal and glial SOCS3 resulted in greater phosphorylation and activation of STAT3, which led to increased expression of its gene target Vegfa, and increased endothelial cell proliferation. In summary, SOCS3 in neurons and glial cells inhibited the STAT3-mediated secretion of VEGF from these cells, which suppresses endothelial cell activation, resulting in decreased endothelial cell proliferation and angiogenesis. These results suggest that neuronal and glial cell SOCS3 limits pathological retinal angiogenesis by suppressing VEGF signaling.
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Registered trials
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