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. 2015 Jun 20;22(18):1633–1645. doi: 10.1089/ars.2014.6078

FIG. 7.

FIG. 7.

Effects of IsoLG-PE are dependent on RAGE. (A) sRAGE (2 mg/L) inhibits activation of NFκB by IsoLG-PE. Results are shown as mean±SEM of all replicates from experiments on 2 separate days, n=4 independent replicates per day, and normalized to expression in cells treated with 0.1 μM PE only. One-way ANOVA, p<0.0001, Bonferroni's multiple-comparisons test *p<0.05 versus 0.1 μM PE, #p<0.05 for sRAGE treatment versus nontreatment with the same concentration of IsoLG-PE. (B) The synthetic glycosaminoglycan, GM-0111 (100 μM), that acts as an antagonist of RAGE also inhibits NFκB activation by IsoLG-PE. One-way ANOVA, p<0.0001, Bonferroni's multiple-comparisons test *p<0.05 versus 0.1 μM PE, #p<0.05 for GM-0111 treatment versus nontreatment with the same concentration of IsoLG-PE. (C) The high-affinity RAGE-specific antagonist, FPS-ZM1 (0.2 μM) inhibits IsoLG-PE-induced NFκB reporter activity. Results are shown as mean±SEM of all replicates from experiments on 3 separate days, n=4–5 independent replicates per day. One-way ANOVA, p<0.0001, Bonferroni's multiple-comparisons test *p<0.05 versus 0.1 μM PE, #p<0.05 for FPS-ZM1 treatment versus nontreatment with the same concentration of IsoLG-PE. sRAGE, soluble form of receptor for advanced glycation endproducts.