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. 2023 May 3;12(9):1308. doi: 10.3390/cells12091308

Figure 3.

Figure 3

A1AT prevents increase in VEGF levels induced by elastase. (A) ELISA-based detection of extracellular VEGF protein levels in the apical and the basal supernatants collected from ARPE-19 monolayers treated with neutrophil elastase (NE) and A1AT for 24 h (n = 3–4). (B) VEGFA mRNA expression in ARPE-19 monolayers treated with NE for 3 h (n = 4) (C) Western blot detection of VEGFA protein and its quantification (D) in the retinas of WT, JR5558 and A1AT injected JR5558 mice (n = 4 retinas per group). (E) FITC dextran permeability assay in NE- and A1AT-treated ARPE-19 monolayers (n = 4) (F) ELISA-based VEGF protein level analysis in the basal supernatants collected from NE and VEGF receptor inhibitor ND (Nintedanib) treated ARPE-19 cells (n = 3–4). (G) ELISA-based VEGF protein level analysis in the basal supernatants collected from NE and PAR 2 antagonist (ENMD 1068) treated ARPE-19 cells. Extracellular C3a (H) and C5a (I) protein levels in NE and A1AT treated ARPE-19 cells (n = 3–4). Statistics used: (A–G) t-test for single comparison, one-way ANOVA, Dunnett’s MC; (H,I) Mann-Whitney non-parametric test. * p < 0.05, ** p < 0.01, **** p < 0.0001, ns: not significant. Data represent the mean ± SEM.