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. 2017 May 23;7:2255. doi: 10.1038/s41598-017-01828-8

Figure 2.

Figure 2

Upregulated expression of chemokines and adhesion molecules in aortas of Apoe / Il27ra /mice. (A,B) Relative gene expression of adhesion molecules ICAM-1 and VCAM-1 in aortas of Apoe / Il27ra / (n = 5) mice fed with WD for 7 weeks (A) or 18 weeks (B) were normalized to L-32 and fold induction was calculated based on the gene expression in aortas of control Apoe / Il27ra +/ (n = 5) mice. (C,D) Relative gene expression of CCL2 and CCL5 in aortas of Apoe / Il27ra / (n = 5) mice fed with WD for 7 weeks (C) or 18 weeks (D) were normalized to L-32 gene expression and fold induction was calculated based on the gene expression in aortas of control Apoe / Il27ra +/ (n = 5) mice. (E,F) CCL2 and CCL5 were measured by multiplex cytokines array in supernatants obtained from aortic cell suspensions of Apoe / Il27ra +/ (n = 5) or Apoe / Il27ra / (n = 5) mice fed with WD for 7 weeks (E) or 18 weeks (F) stimulated with anti-CD3/anti-CD28 for 48 hours. (G) Relative gene expression of vascular adhesion molecule VCAM-1, P-selectin, E-selectin and PECAM-1 in endothelial cells (mLEC cell line) treated with acLDL (100 μg/ml) and rIL-27 (25ng/ml) were normalized to L-32 and fold induction was calculated based on the gene expression in untreated endothelial cells. Data are mean ± SEM from at least 2 independent experiments.