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. 2017 Jan 6;6(1):e004387. doi: 10.1161/JAHA.116.004387

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© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Wls‐deficient infarct macrophages show increased reparative and proangiogenic properties after MI. A1 through A8, Infarct macrophages with Wls deletion display a proangiogenic and antifibrotic cytokine secretion profile. A Magnetic Mouse Bioplex screening assay was performed using conditioned media from Wls‐deficient and control infarct macrophages isolated 4 days after MI. Wls‐deficient macrophages secreted higher levels of the proangiogenic VEGF (A1), IL‐2 (A2), and IL‐6 (A3) cytokines (n=4 in each group) and lower levels of IL‐1α (A4), bFGF (A5), and IL‐13 (A6) compared with controls (n=4 in cfms‐icre;Wls ^fl/fl and n=3 in the control group). There was no difference in the levels of IL‐10 (A7) or MCP‐1 (A8) between the conditioned media of Wls‐deficient and control macrophages. To support the secretome data, the angiogenic capacity of conditioned media from macrophages lacking Wls was determined by HUVEC tube formation assay. B1, Wls‐deficient macrophages are proangiogenic and induced 31% more HUVEC tube formations compared with controls. B2 and B3, Representative images of the matrigel tube formation assay, which show an increased number of vessel‐like formations in the Wls‐deficient macrophage‐conditioned medium group, ×4 magnification (n=8 in cfms‐icre;Wls ^fl/fl and n=7 in the control group). C1 through C3, qPCR analysis of reparative gene expression in isolated cardiac macrophages from cfms‐icre;Wls ^fl/fl and Wls ^fl/fl 4 days after MI. Wls‐deficient macrophages express higher levels of iNOS (C1), TGFβ1 (C2), and IGF1 (C3) compared with control macrophages (n=5 in each group). The relative expression is normalized to GAPDH levels. All results are presented as mean±SEM. Statistical analysis: differences between groups were assessed by 2‐tail unpaired t tests. The nonparametric Mann‐Whitney test was used if data were not normally distributed. bFGF indicates basic fibroblast growth factor; cfms, colony‐stimulating factor 1 receptor; IGF‐1, insulin‐like growth factor 1; IL, interleukin; iNOS, inducible nitric oxide synthase; MI, myocardial infarction; Mφ, macrophage; TGFβ1, transforming growth factor β1; VEGF, vascular endothelial growth factor; Wls, Wntless.