TGF-β–dependent pathogenesis of mitral valve prolapse in a mouse model of Marfan syndrome
J. Clin. Invest. 114:11 doi:10.1172/JCI22715
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Figure 3

Phenotypic rescue after TGF-β antagonism. (A) Morphometric analysis of mitral valve length at P6.5 in untreated (control) mice, in mice receiving irrelevant IgG (IgG), and in mice receiving TGF-β–;neutralizing Ab (NeuAb). Leaflet length was significantly shorter in neuAb-treated mice. (B) Morphometric analysis of mitral valve thickness after TGF-β antagonism. Valves from NeuAb-treated mice were significantly less thick than those from IgG-treated counterparts for all genotypes Error bars indicated 95% confidence intervals. *P –; 0.005 vs. IgG; P –; 0.01 vs. IgG.