Figure 18.

IL‐1β neutralization suppresses angiogenesis, inflammatory responses and expression of matrix metalloproteinases in the heart at 2 weeks after TAC. A through G, Mice were analyzed at 2 weeks after TAC or sham operation under treatment of anti‐IL‐1β antibodies (Ab) or control antibodies. A, Immunohistochemistry using antibodies to CD31. The number of vessels per cardiomyocyte was measured in 50 cardiomyocytes (n=3). Scale bars=20 μm. B, Expression levels of vascular endothelial growth factor A (Vegfa) mRNA (n=3). C, Macrophage infiltration. Macrophage density was assessed in heart sections with anti–Mac‐3 staining (n=3). Scale bars=20 μm. D, Expression levels of monocyte chemotactic protein‐1 (Mcp1) mRNA (n=3). E, mRNA expression of matrix metalloproteinases 2 (Mmp2) and 9 (Mmp9) (n=3). F, NF‐κB activity in the heart (n=3). Free p65 levels in the nucleus were measured. Values were normalized to protein levels. G, mRNA expression levels of IL‐1β (Il1β), IL‐6 (Il6), and TNF‐α (Tnfα) in the heart (n=3). Expression levels of each gene were normalized to those of GAPDH (Gapdh). *P<0.05 vs sham; ^†P<0.05 vs control antibodies. IL indicates interleukin; GAPDH, glyceraldehyde‐3‐phosphate dehydrogenase; TAC, transverse aortic constriction; TNF, transforming growth factor.