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. 2022 Jul 14;150(3):594–603.e2. doi: 10.1016/j.jaci.2022.06.020

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Fig 4 — AngII induces ROS monocytic production and DNA damage. Fluorescence in monocytes from an HD, preincubated or not (^...) with LPS (^---) or AngII (^___) (A), AngII (^___) or DPI and AngII (^---) (B), AngII (^___), or losartan and AngII (^---), and exposed to DCFH-DA (C). D, Plasma levels of AngII in patients and controls. Kruskal-Wallis test P = .001. E, Correlation between plasma levels of AngII and monocytic ROS production in patients and controls. F-H, AngII-activated monocytes induce DNA damage in neighboring cells. Ability of HD monocytes stimulated (monocytes/AngII) or not (monocytes) by AngII to cause γ-H2AX foci in bystander BJ cells (F and G) and HD PBMCs (H). The effect of the preincubation of monocytes with DPI (monocytes/DPI + AngII) (F) or AT1 antagonist (monocytes/anti-AT1 + AngII (G) is shown. F, Welch ANOVA P < .001; G and H, Kruskal-Wallis test P < .001. I, Correlation between plasma levels of AngII and the ability of patient PBMCs to induce DNA damage, expressed as the ratio of the percentage of BJ cells presenting γ-H2AX foci in the presence of patient PBMCs to the percentage of BJ cells presenting γ-H2AX foci in the presence of HD PBMCs. J, Correlation between monocytic ROS production and the percentage of T lymphocytes expressing Fas in patients.