FIGURE 6.

Tissue repair of infarcted hearts. A,B, Masson's trichrome staining of ventricular chamber dilatation and wall thinning, with collagen deposition (blue), in representative infarcted myocardial sections without cell treatment (eCP[−], 2 months postinfarction, right panels in A). Intramyocardial delivery of eCP cells (eCP[+], 600 000 cells per heart), following myocardial infarction, blunted cardiomyopathic features. Scale bar = 1 mm. Numbers of animals were five per group. C‐E, Immunohistochemistry of infarcted heart regions showed significant increase in CD31 and SMA staining in eCP treated mice, respective markers of endothelial and smooth muscle cells, and decrease in TGFβ1 staining, a marker of collagen synthesis and fibrotic processes. Fold change was normalized to eCP(−) infarcted heart counterparts. Scale bar = 100 μm; *P < .05; **P < .01; ***P < .001 with Mann‐Whitney test (≥17 left ventricular sections per group with five animals per group and ≥3 sections per animal). TGFβ1, transforming growth factor β1. SMA, smooth muscle actin