scholarly journals BMP4 is required in the anterior heart field and its derivatives for endocardial cushion remodeling, outflow tract septation, and semilunar valve development

2008 ◽  
Vol 237 (11) ◽  
pp. 3200-3209 ◽  
Author(s):  
David J. McCulley ◽  
Ji-One Kang ◽  
James F. Martin ◽  
Brian L. Black
2005 ◽  
Vol 287 (1) ◽  
pp. 134-145 ◽  
Author(s):  
Michael P. Verzi ◽  
David J. McCulley ◽  
Sarah De Val ◽  
Evdokia Dodou ◽  
Brian L. Black

Development ◽  
2007 ◽  
Vol 134 (8) ◽  
pp. 1593-1604 ◽  
Author(s):  
M. M. Goddeeris ◽  
R. Schwartz ◽  
J. Klingensmith ◽  
E. N. Meyers

2012 ◽  
Vol 52 (5) ◽  
pp. 1096-1102 ◽  
Author(s):  
Chieh-Yu Lin ◽  
Chien-Jung Lin ◽  
Chen-Hao Chen ◽  
Richard M. Chen ◽  
Bin Zhou ◽  
...  

2021 ◽  
Vol 8 (4) ◽  
pp. 42
Author(s):  
Sonia Stefanovic ◽  
Heather C. Etchevers ◽  
Stéphane Zaffran

Anomalies in the cardiac outflow tract (OFT) are among the most frequent congenital heart defects (CHDs). During embryogenesis, the cardiac OFT is a dynamic structure at the arterial pole of the heart. Heart tube elongation occurs by addition of cells from pharyngeal, splanchnic mesoderm to both ends. These progenitor cells, termed the second heart field (SHF), were first identified twenty years ago as essential to the growth of the forming heart tube and major contributors to the OFT. Perturbation of SHF development results in common forms of CHDs, including anomalies of the great arteries. OFT development also depends on paracrine interactions between multiple cell types, including myocardial, endocardial and neural crest lineages. In this publication, dedicated to Professor Andriana Gittenberger-De Groot and her contributions to the field of cardiac development and CHDs, we review some of her pioneering studies of OFT development with particular interest in the diverse origins of the many cell types that contribute to the OFT. We also discuss the clinical implications of selected key findings for our understanding of the etiology of CHDs and particularly OFT malformations.


2019 ◽  
Vol 28 (14) ◽  
pp. 2295-2308 ◽  
Author(s):  
Daniela Alfano ◽  
Alessandra Altomonte ◽  
Claudio Cortes ◽  
Marchesa Bilio ◽  
Robert G Kelly ◽  
...  

Abstract Tbx1, the major candidate gene for DiGeorge or 22q11.2 deletion syndrome, is required for efficient incorporation of cardiac progenitors of the second heart field (SHF) into the heart. However, the mechanisms by which TBX1 regulates this process are still unclear. Here, we have used two independent models, mouse embryos and cultured cells, to define the role of TBX1 in establishing morphological and dynamic characteristics of SHF in the mouse. We found that loss of TBX1 impairs extracellular matrix (ECM)-integrin-focal adhesion (FA) signaling in both models. Mosaic analysis in embryos suggested that this function is non-cell autonomous, and, in cultured cells, loss of TBX1 impairs cell migration and FAs. Additionally, we found that ECM-mediated integrin signaling is disrupted upon loss of TBX1. Finally, we show that interfering with the ECM-integrin-FA axis between E8.5 and E9.5 in mouse embryos, corresponding to the time window within which TBX1 is required in the SHF, causes outflow tract dysmorphogenesis. Our results demonstrate that TBX1 is required to maintain the integrity of ECM-cell interactions in the SHF and that this interaction is critical for cardiac outflow tract development. More broadly, our data identifies a novel TBX1 downstream pathway as an important player in SHF tissue architecture and cardiac morphogenesis.


PLoS ONE ◽  
2009 ◽  
Vol 4 (7) ◽  
pp. e6267 ◽  
Author(s):  
Francesca Rochais ◽  
Mathieu Dandonneau ◽  
Karim Mesbah ◽  
Thérèse Jarry ◽  
Marie-Geneviève Mattei ◽  
...  

2020 ◽  
Vol 143 ◽  
pp. 51-62 ◽  
Author(s):  
Adèle Faucherre ◽  
Hamid Moha ou Maati ◽  
Nathalie Nasr ◽  
Amélie Pinard ◽  
Alexis Theron ◽  
...  

2008 ◽  
Vol 313 (1) ◽  
pp. 25-34 ◽  
Author(s):  
Fanny Bajolle ◽  
Stéphane Zaffran ◽  
Sigolène M. Meilhac ◽  
Mathieu Dandonneau ◽  
Ted Chang ◽  
...  

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