Myocardin regulates expression of contractile genes in smooth muscle cells and is required for closure of the ductus arteriosus in mice
J. Clin. Invest. Jianhe Huang, et al. 118:515 doi:10.1172/JCI33304 [Go to this article.]

Figure 2
Wnt1-Cre mediated recombination in neural crest–derived SMCs. (A and B) Wnt1-Cre transgenic mice were interbred with R26R mice to define pattern of Cre-mediated gene excision. (A) P2 R26R⁺ control mouse demonstrating normal patterning of the cardiac outflow tract and great arteries, pulmonary artery (PA), DA, ascending aorta (AAo), descending aorta (DAo), carotid arteries (CA), and subclavian artery (SC). Original magnification, ×10. (B) P2 Wnt1-Cre⁺/R26R⁺ mouse demonstrating β-galactosidase expression (blue stain) in arteries populated by neural crest–derived SMCs. Original magnification, ×10. (C) Transverse section of P2 Wnt1-Cre⁺/R26R⁺ mouse demonstrating the AAo. Most but not all SMCs populating the AAo stain blue. Original magnification, ×200. (D) Transverse section of P2 Wnt1-Cre⁺/R26R⁺ mouse demonstrating robust Wnt1-Cre–mediated recombination in the DA. Original magnification, ×100. (E and F) Frontal sections of an E11.5 Wnt1-Cre⁺/R26R⁺ embryo demonstrating β-galactosidase activity restricted to the endocardial cushions in the right ventricle (RV) (F) and the AAo and DA (E). Original magnification, ×100. (G–J) Immunohistochemical analyses performed with anti-myocardin antibody demonstrating markedly diminished myocardin expression (brown nuclear stain) in the SMCs populating the internal carotid artery (ICA) (G and H) and aorta (Ao) (I and J) of P2 Myocd^F/F/Wnt1-Cre⁺ mutant mice (H and J) compared with a control Myocd^F/F littermate (G and I). Original magnification, ×300 (carotid); ×400 (aorta).