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. 2018 Jun 20;32(12):6358–6370. doi: 10.1096/fj.201800691R

Figure 2.

Figure 2

NETs formed in the myocardium after I/R injury contribute to myocardial infarction in mice. A) Immunofluorescence microscopy revealed that Gr-1–positive neutrophils (pink) are releasing H3Cit-positive NETs (yellow) in the infarcted myocardium of wild-type (WT) mice. Arrow indicates a NET. B) Triphenyltetrazolium chloride (TTC) staining of cross-sections of the left ventricle at 24 h after myocardial I/R injury (top). Infarcted areas appear as white tissue are outlined with dotted lines. Summarized data of left ventricle infarct size, expressed as the percentage of left ventricle (LV; bottom). The infarct size is remarkably smaller in PAD4−/− mice compared with WT mice. Systemic treatment with DNase 1 does not further reduce the infarct size of PAD4−/− mice, which indicates that the extracellular DNA in the damaged heart predominantly originates from NETs. From Savchenko et al. (57). Reprinted with permission from the American Society of Hematology.