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. 2008 Feb 1;118(2):515–525. doi: 10.1172/JCI33304

Figure 5. MyocdF/F/Wnt1-Cre+ mutant mice exhibit a generalized defect in vascular SMC differentiation.

Figure 5

(A, D, G, and J) Serial histological sections of the AAo of an E16.5 MyocdF/F control mouse. (A) H&E-stained AAo. (D, G, and J) Robust expression of SMA (D), SM-MyHC (G), and SM22α (J) is observed. (B, E, H, and K) Serial histological sections showing the AAo of an E16.5 MyocdF/F/Wnt1-Cre+ mutant mouse. (B) H&E-stained AAo. (E, H, and K) Expression of SMA (E), SM-MyHC (H), and SM22α (K) is markedly diminished in the AAo of MyocdF/F/Wnt1-Cre+ mutant mouse. (C, F, I, and L) Serial histological sections showing the DAo of an E16.5 MyocdF/F/Wnt1-Cre+ mutant mouse. (C) H&E-stained section of the DAo. (F, I, and L) Robust expression of SMA (F), SM-MyHC (I), and SM22α (L) is observed in the DAo of a MyocdF/F/Wnt1-Cre+ mutant mouse. Original magnification, ×200. (M) RT-PCR analysis of SMC contractile gene expression in MyocdF/F/Wnt1-Cre+ mutant and control mice. mRNA harvested from the proximal aorta, carotid arteries, and DA of 4 P2 MyocdF/F/Wnt1-Cre+ mice and 4 control mice was analyzed for expression of GAPDH, SMA, calponin-h1 (calponin), SM-MyHC, and SM22α by real-time RT-PCR as described (28). Data are expressed as mean gene expression (arbitrary units) ± SEM. Gray bars represent gene expression in MyocdF/F/Wnt1-Cre+ mutant mice and black bars represent gene expression in control mice.