ArticleFrontiers in pharmacology2022
Retinal microglia protect against vascular damage in a mouse model of retinopathy of prematurity.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Polyunsaturated Fatty Acid Balance Modulates Microglial State in a Murine Model of Oxygen-Induced Neovascularization.Nutrients · 2026Article
- FoxO1, together with Notch1, promotes microglial activation to induce pathological changes in the retinal vasculature under hypoxia.Cellular and molecular life sciences : CMLS · 2025Article
- Polyunsaturated fatty acid balance modulates microglial state in a murine model of oxygen-induced neovascularization.Research square · 2025Article
- Modulation of microglial phagocytosis via the GAS6-MERTK pathway regulates pathological angiogenesis in the mouse oxygen-induced retinopathy model.Cell death & disease · 2025Article
- High-resolution multimodal visible light optical coherence tomography and scanning laser ophthalmoscopy forBiomedical optics express · 2025Article
- IC100, a humanized therapeutic monoclonal anti-ASC antibody alleviates oxygen-induced retinopathy in mice.Angiogenesis · 2024Article
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions.Journal of neuroinflammation · 2024Review
- Ocular Vascular Diseases: From Retinal Immune Privilege to Inflammation.International journal of molecular sciences · 2023Review
- Microglia: The breakthrough to treat neovascularization and repair blood-retinal barrier in retinopathy.Frontiers in molecular neuroscience · 2023Review
- Article
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6 authors.
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Abstract
Retinopathy of prematurity (ROP) is a common cause of blindness in preterm babies. As a hypoxia-induced eye disease characterized by neovascularization, its association with retinal microglia has been noted but not well documented. We performed a comprehensive analysis of retinal microglia and retinal vessels in mouse oxygen-induced retinopathy (OIR), an animal model of ROP. In combination with a pharmacological inhibitory strategy, the role of retinal microglia in vascular network maintenance was investigated. Postnatal day (P) 7 C57BL/6J mouse pups with their nursing mother were exposed to 75% oxygen for 5 days to induce OIR. Age-matched room air-treated pups served as controls. On P12, P17, P21, P25, and P30, retinal microglia and vessels were visualized and quantified based on their location and activation status. Their relationship with retinal vessels was also analyzed. On P5 or P12, retinal microglia inhibition was achieved by intravitreal injection of liposomes containing clodronate (CLD); retinal vasculature and microglia were examined in P12 and P17 OIR retinae. The number of retinal microglia was increased in the superficial areas of OIR retinae on P12, P17, P21, P25, and P30, and most of them displayed an amoeboid (activated) morphology. The increased retinal microglia were associated with increased superficial retinal vessels in OIR retinae. The number of retinal microglia in deep retinal areas of OIR retinae also increased from P17 to P30 with a ramified morphology, which was not associated with reduced retinal vessels. Intravitreal injection of liposomes-CLD caused a significant reduction in retinal microglia. Loss of retinal microglia before hyperoxia treatment resulted in increased vessel obliteration on P12 and subsequent neovascularization on P17 in OIR retinae. Meanwhile, loss of retinal microglia immediately after hyperoxia treatment on P12 also led to more neovascularization in P17 OIR retinae. Our data showed that activated microglia were strongly associated with vascular abnormalities upon OIR. Retinal microglial activation continued throughout OIR and lasted until after retinal vessel recovery. Pharmacological inhibition of retinal microglia in either hyperoxic or hypoxic stage of OIR exacerbated retinal vascular consequences. These results suggested that retinal microglia may play a protective role in retinal vasculature maintenance in the OIR process.
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