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. 2023 Jun 12;17:1192464. doi: 10.3389/fncel.2023.1192464

FIGURE 2.

FIGURE 2

Dual angiopoietin-2 (Ang-2)/vascular endothelial growth factor-A (VEGF-A) inhibition causes sustained spontaneous choroidal neovascularization (CNV) and lesion leakage area reduction in JR5558 mice. (A) General experimental protocol used to assess long-term treatments effects on limiting vascular leakage, neovascularization, and inflammation in the JR5558 spontaneous CNV mouse model. (B) Representative analysis by immunofluorescence staining of isolectin B4 signal on retinal pigment epithelium (RPE)/choroid flatmounts in JR5558 mice 5 weeks after treatment with immunoglobulin G (IgG) control or anti–VEGF-A, anti–Ang-2, or bi-specific anti–Ang-2/VEGF-A antibodies. Scale bar = 500 μm. (C) Total area of isolectin B4 signal on RPE/choroid whole flatmounts in JR5558 mice 5 weeks after treatment with IgG control or anti–VEGF-A, anti–Ang-2, or bi-specific anti–Ang-2/VEGF-A antibodies (n = 20–22 flatmounts). (D) Representative infrared (IR) and fluorescein angiography (FA) images showing CNV leakage in JR5558 mice at day (D) 43 after treatment with IgG control or anti–VEGF-A, anti–Ang-2, or bi-specific anti–Ang-2/VEGF-A antibodies. (E) Lesion leakage area quantification in JR5558 mice 5 weeks after treatment with IgG control or anti–VEGF-A, anti–Ang-2, or bi-specific anti–Ang-2/VEGF-A antibodies (n = 17–18 eyes). Values are mean ± SD. One-way analysis of variance followed by Tukey’s multiple comparison test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. IHC, immunohistochemistry.