Key result
VEGF120/120 embryos exhibited a disorganized Nkx2.5-positive mesenchymal population along the pulmonary outflow tract compared to the asymmetric elongated column in wild type embryos.
May inform mechanisms of outflow tract defects; leaves open relevance to human congenital heart disease.
BACKGROUND: Understanding of cardiac outflow tract (OFT) remodeling is essential to explain repositioning of the aorta and pulmonary orifice. In wild type embryos (E9.5-14.5), second heart field contribution (SHF) to the OFT was studied using expression patterns of Islet 1, Nkx2.5, MLC-2a, WT-1, and 3D-reconstructions. Abnormal remodeling was studied in VEGF120/120 embryos. RESULTS: In wild type, Islet 1 and Nkx2.5 positive myocardial precursors formed an asymmetric elongated column almost exclusively at the pulmonary side of the OFT up to the pulmonary orifice. In VEGF120/120 embryos, the Nkx2.5-positive mesenchymal population was disorganized with a short extension along the pulmonary OFT. CONCLUSIONS: We postulate that normally the pulmonary trunk and orifice are pushed in a higher and more frontal position relative to the aortic orifice by asymmetric addition of SHF-myocardium. Deficient or disorganized right ventricular OFT expansion might explain cardiac malformations with abnormal position of the great arteries, such as double outlet right ventricle.
No takes yet. Share an insight, caveat, or question.
Scherptong et al. (2012) studied Cardiac outflow tract remodeling. VEGF120/120 mutation vs. Wild type embryos was evaluated on Cardiac outflow tract remodeling and expression patterns of myocardial precursors. VEGF120/120 embryos exhibited a disorganized Nkx2.5-positive mesenchymal population along the pulmonary outflow tract compared to the asymmetric elongated column in wild type embryos.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: