Fig. 3

AIP1 overexpression decreases neovascularization, ROS production, and NOX4 expression and alleviates the imbalance in NLRP3/NLRP6. A Western blot analysis showing that AIP1 was significantly upregulated in AIP1-overexpressing mice compared with that in control mice after alkali burn injury (N = three). B Representative slit-lamp images showing that AIP1 overexpression notably decreased neovascularization compared with that in the control group (magnification: × 40). C Corneal whole-mount staining showing that AIP1 overexpression notably decreased neovascularization compared with that in the control group (scale bar: 1 mm). D The corneal opacity, neovessel size, and vessel size scores decreased significantly in AIP1-overexpressing mice compared with those in control mice after alkali burn injury (N = nine). E The DCFDA ROS assay revealed that AIP1 overexpression notably decreased the ROS production observed after alkali burn injury compared with that in the control group (scale bar: 100 μm). F RT–qPCR showed that AIP1 overexpression significantly abrogated the reduction in NLRP6 and decreased the elevation in NOX4, NLRP3 and VEGFa induced by alkali burn injury (N = three). G Western blot analysis showed that AIP1 overexpression significantly abrogated the reduction in NLRP6 and decreased the elevation in NOX4 and NLRP3 induced by alkali burn injury (N = three). H Immunofluorescence staining showed that AIP1 overexpression significantly decreased the elevation in VEGFa induced by alkali burn injury (scale bar: 50 μm; magnification: × 400). I Immunoprecipitation analysis showed that AIP1 could bind directly to NOX4 in 293 T cells (N = three). 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