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Morphogenesis of outflow tract rotation during cardiac development: The pulmonary push concept
Author(s) -
Scherptong Roderick W.C.,
Jongbloed Monique R.M.,
Wisse Lambertus J.,
VicenteSteijn Rebecca,
Bartelings Margot M.,
Poelmann Robert E.,
Schalij Martin J.,
GittenbergerDe Groot Adriana C.
Publication year - 2012
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.23833
Subject(s) - ventricle , biology , body orifice , anatomy , medicine , aorta , heart development , cardiology , morphogenesis , pulmonary valve , embryo , atrioventricular cushions , great arteries , embryonic stem cell , microbiology and biotechnology , heart disease , biochemistry , gene
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. Developmental Dynamics 241:1413–1422, 2012. © 2012 Wiley Periodicals, Inc.