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. 2020 Jun 29;11:3273. doi: 10.1038/s41467-020-16923-0

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a Representative 180 min reperfused infarct at 1 week post-infarction shows regions of iron accumulation at the transition zone between myocyte necrosis and mixed viable myocytes (Prussian blue, black, and blue arrows) colocalized with MHC class II antigen-presenting cells (Cathepsin-S, black arrows) and newly recruited macrophages (MAC-387, blue arrows). b, c Representative permanently occluded infarct at 1 week post-infarction also had heterogeneous macrophage aggregation with newly recruited macrophages (MAC-387, blue arrows) and MHC class II antigen-presenting cells (Cathepsin-S, black arrows) colocalized with iron accumulation (Prussian blue, black, and blue arrows). Histology was repeated in independent tissue sections for 90 (n = 2), 180 min (n = 2) reperfused, and permanent (n = 2) infarcts which showed similar histopathological findings within reperfused and permanent infarct groups. a and b are at ×40 magnification and c is at ×100 magnification.