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Fig. 1 | Journal of Inflammation

Fig. 1

From: Peroxisome proliferator-activated receptor (PPAR) α and δ activators induce ICAM-1 expression in quiescent non stimulated endothelial cells

Fig. 1

Effects of PPARα and δ agonists on the ICAM-1 surface and protein expression as well as funtion in non-stimulated HUVEC. a Flow-cytometric analyses of ICAM-1 expression; HUVECs were left untreated (solvent only) or were treated with different concentrations of PPARα agonsist (WY14643 (100 and 200 μM) and Fenofibrate (100 and 200 μM) or PPARδ agonists (L-165041 (25 and 50 μM) and GW501514 (10 and 20 μM)). As positive control TNFα (20 ng/ml) was used. Mean values from triplicate experiments performed four times are depicted ± SEM. *p < 0.05 was considered significant. Exemplary plots for the PPARα agonist WY14643 and the PPARδ agonist GW601514 are depicted. b Representative western blot analyses of endothelial cells that were left untreated (solvent only) or were treated with WY14643 and L-165041 for 24 h at different concentrations. Comparable results were obtained from three independent experiments. The results were normalized to the expression of tubulin. The relative expression of ICAM-1 is presented in % of control. The mean values from three independent experiments are presented as the mean ± SEM. *p < 0.05. c Representative western blot analyses of endothelial cells that were left untreated (solvent only) or were treated with WY14643 (200 μM) and L-165041 (50 μM) at different time points. Comparable results were obtained from three independent experiments. The results were normalized to the expression of tubulin. The relative expression of ICAM-1 is presented in % of control. The mean values from three independent experiments are presented as the mean ± SEM. *p < 0.05. d Adhesion assay for the functional interaction between T cells (Jurkat) and endothelial cells: HUVECs were left untreated (solvent only) or were treated with PPARδ agonists for 24 h (L-165041 (50 μM) and GW501514 (20 μM)) or (e) PPARα agonists for 24 h (Fenofibrat (100 μM) and WY14643 (200 μM)). As positive control TNFα (20 ng/ml) was used. Jurkat cells were allowed to adhere to the endothelial cells for 3 min following stepwise increase of shear stress. The number of adherent cells was quantified. The mean values from five independent experiments are presented as the mean ± SEM. *p < 0.05 was considered significant

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