Key result
Id2 knockout in mouse embryos resulted in severe cardiac defects, including abnormal orientation of systemic and pulmonary drainage, ventricular septal defects, and myocardial hypoplasia.
Id2 is essential for normal cardiac development, specifically contributing to the second heart field at both the arterial and venous poles.
Hypothesis-generating for genetic mechanisms in human congenital heart disease; requires validation before any clinical relevance.
The inhibitor of differentiation Id2 is expressed in mesoderm of the second heart field, which contributes myocardial and mesenchymal cells to the primary heart tube. The role of Id2 in cardiac development is insufficiently known. Heart development was studied in sequential developmental stages in Id2 wildtype and knockout mouse embryos. Expression patterns of Id2, MLC-2a, Nkx2.5, HCN4, and WT-1 were analyzed. Id2 is expressed in myocardial progenitor cells at the inflow and outflow tract, in the endocardial and epicardial lineage, and in neural crest cells. Id2 knockout embryos show severe cardiac defects including abnormal orientation of systemic and pulmonary drainage, abnormal myocardialization of systemic and pulmonary veins, hypoplasia of the sinoatrial node, large interatrial communications, ventricular septal defects, double outlet right ventricle, and myocardial hypoplasia. Our results indicate a role for Id2 in the second heart field contribution at both the arterial and the venous poles of the heart.
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Jongbloed et al. (2011) studied Cardiac development. Id2 knockout vs. Id2 wildtype was evaluated on Cardiac defects and expression patterns. Id2 knockout in mouse embryos resulted in severe cardiac defects, including abnormal orientation of systemic and pulmonary drainage, ventricular septal defects, and myocardial hypoplasia.
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