ArticleInvestigative ophthalmology & visual science2008
MCP-1 deficiency delays regression of pathologic retinal neovascularization in a model of ischemic retinopathy.
Article in Investigative ophthalmology & visual science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Proliferative diabetic retinopathy subtypes defined by immune defense and endothelial mitochondrial dysfunction.Signal transduction and targeted therapy · 2025Article
- Modulation of microglial phagocytosis via the GAS6-MERTK pathway regulates pathological angiogenesis in the mouse oxygen-induced retinopathy model.Cell death & disease · 2025Article
- Corticosteroids reduce pathological angiogenesis yet compromise reparative vascular remodeling in a model of retinopathy.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Microglia in retinal angiogenesis and diabetic retinopathy.Angiogenesis · 2024Review
- Early Depletion of Neutrophils Reduces Retinal Inflammation and Neovascularization in Mice with Oxygen-Induced Retinopathy.International journal of molecular sciences · 2023Article
- Perilipin 2-positive mononuclear phagocytes accumulate in the diabetic retina and promote PPARγ-dependent vasodegeneration.The Journal of clinical investigation · 2023Article
- Review
- Inhibition of NF-κB ameliorates aberrant retinal glia activation and inflammatory responses in streptozotocin-induced diabetic rats.Annals of translational medicine · 2023Article
- Differential distribution of steroid hormone signaling networks in the human choroid-retinal pigment epithelial complex.BMC ophthalmology · 2022Article
- Harnessing retinal phagocytes to combat pathological neovascularization in ischemic retinopathies?Pflugers Archiv : European journal of physiology · 2022Review
- Retinal microglia protect against vascular damage in a mouse model of retinopathy of prematurity.Frontiers in pharmacology · 2022Article
- The innate immune system in diabetic retinopathy.Progress in retinal and eye research · 2021Review
- Retro-orbital injection of FITC-dextran combined with isolectin B4 in assessing the retinal neovascularization defect.BMC ophthalmology · 2021Article
- Mast cell hyperactivity underpins the development of oxygen-induced retinopathy.The Journal of clinical investigation · 2017Article
- Promoting vascular repair in the retina: can stem/progenitor cells help?Eye and brain · 2016Review
- Article
- Retinal neuronal MCP-1 induced by AGEs stimulates TNF-α expression in rat microglia via p38, ERK, and NF-κB pathways.Molecular vision · 2014Article
- Inhibition of apelin expression switches endothelial cells from proliferative to mature state in pathological retinal angiogenesis.Angiogenesis · 2013Article
- The regulatory roles of apoptosis-inducing factor in the formation and regression processes of ocular neovascularization.The American journal of pathology · 2012Article
- Anti-inflammatory therapy for diabetic retinopathy.Immunotherapy · 2011Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe present study investigates whether retinal neovascularization (NV) and apoptosis are altered in MCP-1-deficient ((-/-)) mice in the OIR model.
methodsPostnatal day (P) 7 MCP-1(-/-) and C57BL/6 (B6) mice were exposed to 75% oxygen for 5 days and then recovered in room air. Immunostaining was performed to localize macrophages/microglia within retinal whole mounts and cross-sections. Retinopathy was qualitatively assessed in FITC-dextran-perfused retinas, and preretinal NV was quantified on P17, P21, and P24. TUNEL analysis was used to compare apoptosis between B6 and MCP-1(-/-) mice.
resultsMCP-1(-/-) and B6 mice revealed normal vascular development in room air controls and similar vaso-obliteration in oxygen-exposed mice on P12. MCP-1(-/-) mice exhibited significantly reduced vascular tuft-associated F4/80(+) cells compared with B6 mice. FITC-dextran-perfused retinas exhibited prominent neovascular tufts on P17, and quantification of preretinal nuclei revealed no significant differences between MCP-1(-/-) and B6 mice. In contrast, on P21 and P24, MCP-1(-/-) mice exhibited significant increases in preretinal neovascular nuclei compared with B6 controls. These increases in NV in the MCP-1(-/-) mice were associated with a significant reduction in vascular tuft apoptosis.
conclusionsThe results demonstrate that the absence of MCP-1 does not alter normal retinal vascular development. Furthermore, MCP-1(-/-) mice exhibit a similar neovascular response on P17. However, the reduction in tuft-associated macrophages/microglia in the MCP-1(-/-) mice correlates with reduced vascular tuft apoptosis and delayed regression of retinal NV. These findings suggest that macrophages/microglia may contribute to tuft regression through their proapoptotic properties.
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