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. 2015 Dec 10;30(1):48–61. doi: 10.1210/me.2015-1176

Figure 1. A20 controls β-cell survival in response to proinflammatory stimuli.

Figure 1.

A and B, A20 mRNA (A) and protein expression (B) after treatment of INS-1E cells with IL-1β+IFN-γ or TNF+IFN-γ for different time points, as indicated. C and D, A20 mRNA (C) and protein expression (D) after treatment of mouse islets with IL-1β+IFN-γ or TNF+IFN-γ for different time points, as indicated. A and C, Data are means ± SEM of 3–5 independent experiments. *, P < .05 IL-1β+IFN-γ vs control; §, P < .05 TNF+IFN-γ vs control. B and D, Representative Western blottings of 4–5 independent experiments are shown. E, Quantification of percentage of apoptosis in INS-1E cells transfected with siRNA control (siCtrl), siA20#1, or siA20#2 and treated with IL-1β+IFN-γ or TNF+IFN-γ for 16 hours. *, P < .05 vs siCtrl condition. F, Quantification of percentage of cell death in islets isolated form WT or A20β-KO mice and exposed to IL-1β+IFN-γ or TNF+IFN-γ for 24 hours. *, P < .05 vs WT. G, Quantification of percentage of apoptosis in dispersed rat islets cells infected with the adenoviruses encoding luciferase (AdCtrl) or A20 (AdA20) at different MOIs and exposed to IL-1β+IFN-γ for 24 hours. *, P < .05 vs AdCtrl treated with cytokines. H, Quantification of percentage of apoptosis in INS-1E cells transfected with siCtrl or siA20#2 and treated with IL-1β, TNF, or IFN-γ for 16 hours. *, P < .05 vs siCtrl. I, Quantification of percentage of cell death in islets isolated form WT or A20β-KO mice and exposed to IL-1β for 24 hours. *, P < .05 vs WT. E–I, Data are means ± SEM of 3–6 independent experiments.