Fig. 2

AIP1 depletion increases neovascularization, ROS production, and NOX4 expression and exacerbates the imbalance in NLRP3/NLRP6. A Representative slit-lamp images showing that AIP1 KO notably increased neovascularization compared with that in C57BL/6 mice (magnification: × 40). B Corneal whole-mount staining showing that AIP1 KO mice exhibited notably increased neovascularization compared with C57BL/6 mice (scale bar: 1 mm). C The corneal opacity, neovessel size, and vessel size scores increased significantly in AIP1-KO mice compared with those in C57BL/6 mice after alkali burn injury (N = nine). D The DCFDA ROS assay revealed that AIP1 KO notably increased ROS production after alkali burn injury compared with that in the control group (scale bar: 100 μm). E RT–qPCR analysis of AIP1 gene knockout efficiency. Deletion of AIP1 significantly increased the reduction in NLRP6 and elevation in NOX4, NLRP3 and VEGFa induced by alkali burn injury (N = three). F Western blot analysis showed that AIP1 deletion significantly increased the reduction in NLRP6 and elevation in NOX4 and NLRP3 induced by alkali burn injury (N = three). G Immunofluorescence staining showing that deletion of AIP1 significantly increased the elevation in VEGFa induced by alkali burn injury (scale bar: 50 μm; magnification: × 400). Error bars represent the mean ± SD, and comparisons were performed using one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001