ArticleBiochemistry and biophysics reports2026
The influence of TLR4 signaling on retinal ganglion cell survival and angiogenic response in a mouse model of oxygen-induced retinopathy.
Article in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: Retinopathy of prematurity (ROP) is a critical concern in neonatal care and potentially leads to vision impairment. Despite advancements in anti-VEGF treatments, the mechanisms driving pathological vitreoretinal neovascularization remain unclear. I examined the role of Toll-like receptor 4 (TLR4) in modulating inflammatory cytokines, angiogenesis, and neuronal cell protection in a mouse model of oxygen-induced retinopathy (OIR). Materials and methods: C57BL/6J TLR4-/- mice were subjected to OIR by exposure to 75% oxygen from postnatal days 7 to 12 (P7 to P12) following approved protocols. I used immunohistochemistry to assess TLR4 expression at P19, real-time quantitative PCR for proinflammatory cytokines at P19, ex vivo fluorescent vascular imaging to evaluate retinal vascular changes at P19, and retinal neuronal cells death evaluated by whole-mounted retina stained with cresyl violet at P47. Statistical significance was determined using one-way ANOVA (p < 0.05). Results: Immunofluorescence demonstrated TLR4 expression in microglia in OIR retinas of wild-type mice but not in controls. Real-time PCR revealed significant upregulation of vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein-1 (MCP1) in OIR retinas, which was mitigated in TLR4-/- mice. Retinal angiogenesis significantly increased in wild-type OIR mice, whereas TLR4 knockdown inhibited these changes. Additionally, OIR caused approximately 30% neuronal cell death in the retinal ganglion cell layer, which was largely prevented in the TLR4-/- mice. Conclusions: These findings underscore TLR4's pivotal role in the regulation of inflammatory responses and angiogenesis in ROP. Targeting TLR4 may represent a novel therapeutic approach to preserve retinal integrity and improve visual outcomes in at-risk populations, particularly in premature infants.
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