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Supplementary Figure LDH [U/l] released in the supernatant Hypoxia (h) * b Supplementary Fig. 1 Macrophages and cardiac fibroblasts exposed to hypoxia. Macrophages (a) and cardiac fibroblasts were exposed to hypoxia (1.5% O 2 ) and LDH was measured in the supernatant at the indicated intervals (*P<0.01) a LDH [U/l] released in the supernatant * * (h) Hypoxia

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10 2 MPO-positive cells/mm 2 GenotypeWTWTRAGE -/- RAGE -/- S100A8/A I/R 10 2 CD68-positive cells/mm 2 GenotypeWTWT RAGE -/- RAGE -/- S100A8/A I/R * * * ** Supplementary Figure 2 Supplementary Fig. 2 Quantification of CD68-positive (a) and MPO-positive (b) cells in infarcted myocardium 28 days post MI. (a) *p>0.001 vs. all other treatment groups, **p>0.001 vs. WT and WT+S100A8/A9 groups. (b) *p>0.05 vs. all other treatment groups, ns=not significant. ab

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GenotypeWTWT RAGE -/- RAGE -/- S100A8/A I/R 10 2 SMA-positive cells/mm 2 Supplementary Figure 3 Supplementary Fig. 3 Quantification of alpha smoot-muscle actin (ASMA)- positive cells in infarcted myocardium 28 days post MI. *p>0.001 vs. all other treatment groups

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LVEDD [mm] ShamMI 7dMI 28 d * ** WT WT + S100A8/A9 RAGE RAGE + S100A8/A9 Supplementary Figure 4 Supplementary Fig. 4 WT- and RAGE –/– mice were subjected to I/R injury. Echocardiographic assessment of the left ventricular end-diastolic diameter (LVEDD) (*P<0.001, **P< vs. WT-sham) at given time points.

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Supplementary Figure 5 Supplementary Fig. 5 Kaplan-Meier-Plot of mice that received ischemia/reperfusion injury and S100A8/A9-treatment as indicated (follow-up for 28 days). Log rank test p=0.861.

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