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Expression of Id2 in the second heart field and cardiac defects in Id2 knock‐out mice
Author(s) -
Jongbloed M.R.M.,
VicenteSteijn R.,
Douglas Y.L.,
Wisse L.J.,
Mori K.,
Yokota Y.,
Bartelings M.M.,
Schalij M.J.,
Mahtab E.A.,
Poelmann R.E.,
GittenbergerDe Groot A.C.
Publication year - 2011
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.22762
Subject(s) - heart development , neural crest , biology , medicine , hypoplasia , ventricle , knockout mouse , tbx1 , embryonic stem cell , cardiology , anatomy , embryo , microbiology and biotechnology , gene expression , receptor , genetics , gene , promoter
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. Developmental Dynamics 240:2561–2577, 2011. © 2011 Wiley Periodicals, Inc.