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. 2014 May 22;3(3):e000841. doi: 10.1161/JAHA.114.000841

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© 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 4. — Temporally targeted inactivation of Hif‐1α causes aorta overriding VSD. Control (Hif‐1α^f/f; β‐actinCre⁻) and cKO (Hif‐1α^f/f; β‐actinCre⁺) E15.5 littermate embryos from a mouse injected with 3 mg of TM at E10.5. Embryos are shown in whole mount (A and B) and in sections (C through J) from anterior to posterior with respect to the heart. The cKO embryo (B) is smaller than control (A). In the cKO the RVOT appears narrowed by mesenchyme (arrowhead) and infundibular muscle (D), and the aorta overrides a VSD (F and H). J, More posteriorly the atrio‐ventricular valves appear normal while the ventricular myocardium is thinned. Scale bars: 500 μm. Ao indicates aorta; cKO, conditional knock‐out; Hif, hypoxia‐inducible transcription factor; LV, left ventricle; LVOT, left ventricular outflow tract; pa, pulmonary artery; RV, right ventricle; RVOT, right ventricular outflow tract; TM, tamoxifen; VSD, ventricular septal defect.