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. Author manuscript; available in PMC: 2016 Nov 28.
Published in final edited form as: Sci Transl Med. 2016 Jun 8;8(342):342ra80. doi: 10.1126/scitranslmed.aaf1435

Fig. 2. Noncirculating signals contribute to expansion of plaque leukocyte recruitment after MI.

Fig. 2

(A) Gating strategy and histograms of leukocyte adhesion molecules on aortic endothelial cells from ApoE−/− mice 3 days after MI or no MI controls. (B) Mean fluorescence intensity (MFI) of adhesion molecules expressed by aortic endothelial cells from animals in (A). Data are means ± SEM (n = 11 to 13 per group from two independent experiments). P values versus no MI are determined by Mann-Whitney U test. (C) Chemokine mRNA in aortic roots from animals in (A). Data are means ± SEM (n = 7 to 8 per group from two independent experiments). P values are determined by Mann-Whitney U test. (D) Experimental setup. ApoE−/− mice were joined in parabiosis, andone parabiontwas infarcted 2 weeks thereafter. Three dayslater, CAM levels on aortic endothelial cells were evaluated by flow cytometry. (E) MFI on aortic endothelial cells from animals in (D) was evaluated by flow cytometry. Data are means normalized to steady-state parabiosis ± SEM (n = 7 per group from two independent experiments). P values compare respective infarcted to noninfarcted parabionts and are determined by two-tailed paired Wilcoxon test.