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. 2014 Dec 17;3(6):e001286. doi: 10.1161/JAHA.114.001286

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© 2014 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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Figure 3. — ATM deficiency results in decreased inflammatory cells in the infarct LV region 1 day post‐MI. Cross‐sections of the heart post‐MI were immunostained using anti‐neutrophil (A and B) and anti‐F4/80 (macrophage; C and D) antibodies. The number of immune‐positive cells was quantified using Bioquant Image analysis software. Quantitative analyses of neutrophils 1 (A) and 3 (B) days post‐MI. Quantitative analyses of macrophages 1 (C) and 3 (D) days post‐MI. ^#P<0.05 vs Sham, ^$P<0.05 vs Non, *P<0.05 vs WT; n=4 to 6. ATM indicates ataxia telangiectasia mutated; hKO, heterozygous knockout; Inf, infarct; LV, left ventricle; MI, myocardial infarction; WT, wild‐type.