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. 2009 Jan 1;20(1):509–520. doi: 10.1091/mbc.E08-03-0274

Figure 6.

Figure 6.

Decreasing the antioxidant capacity of MDSCs decreases the ability of MDSCs to mitigate adverse remodeling after an induced myocardial infarction. MDSCs, DEM-treated MDSCs, or PBS was injected into the infarction site. Animals were sacrificed at 8 wk for histological analysis. (A) Mason trichrome staining was performed to measure fibrosis. Representative images of infarcted hearts injected with MDSCs (A1), MDSCs treated with DEM (A2), and PBS (A3) are shown. Arrowheads indicate the main areas of infarcted myocardium. Note the thin fibrotic walls in A2 and A3 compared with the small area of fibrosis in A1. Infarcted hearts injected with MDSCs had significantly less fibrosis than hearts injected with MDSCs treated with DEM or PBS as measured by the scar tissue ratio (A4). (A2) Bar, 1000 μm. (B) The vascularity of the infarcted area was measured by staining the sections for CD31, an endothelial cell marker. Representative images of the capillary density of the infarcted area of hearts injected with MDSCs (B1), MDSCs treated with DEM (B2), and PBS (B3) are shown. Arrowheads outline the myocardial wall. Note the reduced capillary density in the myocardium in B2 and B3 when compared with B1. The capillary density was measured by counting the number of capillaries per pixel area. The infarcted area of hearts injected with MDSCs had significantly higher capillary densities than hearts injected with MDSCs treated with DEM and PBS (B4). (B2) Bar, 50 μm. (A4 and B4) MDSCs + DEM, n = 6; MDSCs, n = 6; PBS control, n = 5. ANOVA; *p ≤ 0.05; mean values ± SEM.