Figure 6. HGF secreted by hASCs abrogated cardiac myofibroblast differentiation via AT₁R and Smad7.

(a) Anti-HGF negated the anti-fibrotic activity of conditioned medium of hASCs, as indicated by significant (p < 0.05) higher gene expression levels of AT₁R and lower gene expression level of Smad7 in cardiac fibroblasts cultured on 30 kPa substrates and cell culture plate (*p < 0.05 relative to after treatment with conditioned medium of hASCs; ^#p < 0.05 relative to before treatment with conditioned medium of hASCs). (b) Summary of proposed mechanism of matrix stiffness-induced cardiac myofibroblast differentiation and anti-fibrotic effects of undifferentiated hASCs. ECM: extracellular matrix; AT₁R: angiotensin II type 1 receptor; HGF: hepatocyte growth factor; TGF-β1: transforming growth factor beta-1; P-Smad2: phosphorylated Smad2; α-SMA: alpha-smooth muscle actin; Col I: collagen I; Col III: collagen III.