S100A8/A9 is a valuable biomarker and treatment target to detect and modulate neutrophil involvement in myocardial infarction

Figures

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  Figure 1. Neutrophil infiltration and S100A9 presence in the myocardium on day 1 post-MI: (A) Representative images of HE staining of left ventricular sections from the sham and MI groups treated with PBS (MI) or ABR-238901 (MI+ABR), respectively, collected on day 1 after myocardial ischemia (400×); (B) Ly6G-positive staining identifying neutrophil infiltration (400×); (C) S100A9-positive immunohistochemical staining in the same areas as in (A) and (B) (400×). HE: Hematoxylin–Eosin; Ly6G: Lymphocyte antigen 6 family member G6D; MI: Myocardial infarction; PBS: Phosphate-buffered saline

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  Figure 2. Neutrophil infiltration and S100A9 presence in the myocardium on day 3 post-MI: (A) Representative images of HE staining of left ventricular sections from the sham and the two MI groups receiving PBS (MI) or ABR-238901 (MI+ABR) treatment, collected on day 3 post-MI (400×); (B) Ly6G-positive neutrophil staining (400×); (C) S100A9 staining in the same areas as in (A) and (B) (400×

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  Figure 3. The S100A9 presence in the infarcted myocardium reflects neutrophil infiltration and the effect of the treatment. Correlations between neutrophil infiltration, expressed as Ly6G-positive staining, and S100A9 staining in myocardium collected on day 1 (A) and day 3 (B) post-MI. The stained area is reported as an average percentage of left ventricular area on five consecutive sections collected at 300 μm intervals

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  Figure 4. Inhibition of S100A8/A9 signaling reduces the extent of MI on day 3 post-MI: (A) Representative HE staining of cardiac sections from the PBS- and ABR-238901-treated mice, three days after induced MI; (B) Masson’s trichrome staining of fibrous scar formation in the infarcted area; (C) Quantification of MI size, expressed as percentage of left ventricular (LV) volume