scholarly journals Retinoic Acid Regulates Differentiation of the Secondary Heart Field and TGFβ-Mediated Outflow Tract Septation

2010 ◽  
Vol 18 (3) ◽  
pp. 480-485 ◽  
Author(s):  
Peng Li ◽  
Mohammad Pashmforoush ◽  
Henry M. Sucov
Keyword(s):  
Retinoic Acid ◽  
Outflow Tract ◽  
Heart Field ◽  
Secondary Heart Field

scholarly journals Myocardial volume and organization are changed by failure of addition of secondary heart field myocardium to the cardiac outflow tract

2003 ◽  
Vol 228 (2) ◽  
pp. 152-160 ◽  
Author(s):  
T. Mesud Yelbuz ◽  
Karen L. Waldo ◽  
Xiaowei Zhang ◽  
Marzena Zdanowicz ◽  
Jeremy Parker ◽  
...  
Keyword(s):  
Outflow Tract ◽  
Heart Field ◽  
Secondary Heart Field ◽  
Cardiac Outflow

scholarly journals Msx1 and Msx2 regulate survival of secondary heart field precursors and post-migratory proliferation of cardiac neural crest in the outflow tract

2007 ◽  
Vol 308 (2) ◽  
pp. 421-437 ◽  
Author(s):  
Yi-Hui Chen ◽  
Mamoru Ishii ◽  
Jingjing Sun ◽  
Henry M. Sucov ◽  
Robert E. Maxson
Keyword(s):  
Neural Crest ◽  
Outflow Tract ◽  
Cardiac Neural Crest ◽  
Heart Field ◽  
Secondary Heart Field

Pitx2cpatterns anterior myocardium and aortic arch vessels and is required for local cell movement into atrioventricular cushions

Development ◽  
2002 ◽  
Vol 129 (21) ◽  
pp. 5081-5091 ◽  
Author(s):  
Chengyu Liu ◽  
Wei Liu ◽  
Jennifer Palie ◽  
Mei Fang Lu ◽  
Nigel A. Brown ◽  
...  
Keyword(s):  
Aortic Arch ◽  
Pulmonary Veins ◽  
Cell Movement ◽  
Branchial Arch ◽  
Outflow Tract ◽  
Major Function ◽  
Atrioventricular Cushions ◽  
Heart Field ◽  
Left Right Asymmetry ◽  
Secondary Heart Field

Inactivation of the left-right asymmetry gene Pitx2 has been shown, in mice, to result in right isomerism with associated defects that are similar to that found in humans. We show that the Pitx2c isoform is expressed asymmetrically in a presumptive secondary heart field within the branchial arch and splanchnic mesoderm that contributes to the aortic sac and conotruncal myocardium. Pitx2c was expressed in left aortic sac mesothelium and in left splanchnic and branchial arch mesoderm near the junction of the aortic sac and branchial arch arteries. Mice with an isoform-specific deletion of Pitx2c had defects in asymmetric remodeling of the aortic arch vessels. Fatemapping studies using a Pitx2 cre recombinase knock-in allele showed that daughters ofPitx2-expressing cells populated the right and left ventricles,atrioventricular cushions and valves and pulmonary veins. In Pitx2mutant embryos, descendents of Pitx2-expressing cells failed to contribute to the atrioventricular cushions and valves and the pulmonary vein,resulting in abnormal morphogenesis of these structures. Our data provide functional evidence that the presumptive secondary heart field, derived from branchial arch and splanchnic mesoderm, patterns the forming outflow tract and reveal a role for Pitx2c in aortic arch remodeling. Moreover, our findings suggest that a major function of the Pitx2-mediated left right asymmetry pathway is to pattern the aortic arches, outflow tract and atrioventricular valves and cushions.

scholarly journals Conotruncal myocardium arises from a secondary heart field

Development ◽  
2001 ◽  
Vol 128 (16) ◽  
pp. 3179-3188 ◽  
Author(s):  
Karen L. Waldo ◽  
Donna H. Kumiski ◽  
Kathleen T. Wallis ◽  
Harriett A. Stadt ◽  
Mary. R. Hutson ◽  
...  
Keyword(s):  
Heart Development ◽  
Outflow Tract ◽  
Heart Tube ◽  
In Ovo ◽  
Atrioventricular Canal ◽  
Lateral Plate ◽  
Heart Field ◽  
Dorsal Mesocardium ◽  
Heart Fields ◽  
Secondary Heart Field

The primary heart tube is an endocardial tube, ensheathed by myocardial cells, that develops from bilateral primary heart fields located in the lateral plate mesoderm. Earlier mapping studies of the heart fields performed in whole embryo cultures indicate that all of the myocardium of the developed heart originates from the primary heart fields. In contrast, marking experiments in ovo suggest that the atrioventricular canal, atria and conotruncus are added secondarily to the straight heart tube during looping. The results we present resolve this issue by showing that the heart tube elongates during looping, concomitant with accretion of new myocardium. The atria are added progressively from the caudal primary heart fields bilaterally, while the myocardium of the conotruncus is elongated from a midline secondary heart field of splanchnic mesoderm beneath the floor of the foregut. Cells in the secondary heart field express Nkx2.5 and Gata-4, as do the cells of the primary heart fields. Induction of myocardium appears to be unnecessary at the inflow pole, while it occurs at the outflow pole of the heart. Accretion of myocardium at the junction of the inflow myocardium with dorsal mesocardium is completed at stage 12 and later (stage 18) from the secondary heart field just caudal to the outflow tract. Induction of myocardium appears to move in a caudal direction as the outflow tract translocates caudally relative to the pharyngeal arches. As the cells in the secondary heart field begin to move into the outflow or inflow myocardium,they express HNK-1 initially and then MF-20, a marker for myosin heavy chain. FGF-8 and BMP-2 are present in the ventral pharynx and secondary heart field/outflow myocardium, respectively, and appear to effect induction of the cells in a manner that mimics induction of the primary myocardium from the primary heart fields. Neither FGF-8 nor BMP-2 is present as inflow myocardium is added from the primary heart fields. The addition of a secondary myocardium to the primary heart tube provides a new framework for understanding several null mutations in mice that cause defective heart development.

scholarly journals Outflow Tract Formation—Embryonic Origins of Conotruncal Congenital Heart Disease

2021 ◽  
Vol 8 (4) ◽  
pp. 42
Author(s):  
Sonia Stefanovic ◽  
Heather C. Etchevers ◽  
Stéphane Zaffran
Keyword(s):  
Congenital Heart ◽  
Cardiac Development ◽  
Heart Defects ◽  
Dynamic Structure ◽  
Cell Types ◽  
Outflow Tract ◽  
Heart Tube ◽  
Heart Field ◽  
Multiple Cell ◽  
The Many

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.

scholarly journals Zebrafish cardiac development requires a conserved secondary heart field

Development ◽  
2011 ◽  
Vol 138 (11) ◽  
pp. 2389-2398 ◽  
Author(s):  
D. Hami ◽  
A. C. Grimes ◽  
H.-J. Tsai ◽  
M. L. Kirby
Keyword(s):  
Cardiac Development ◽  
Heart Field ◽  
Secondary Heart Field

scholarly journals Tbx1 regulates extracellular matrix-cell interactions in the second heart field

2019 ◽  
Vol 28 (14) ◽  
pp. 2295-2308 ◽  
Author(s):  
Daniela Alfano ◽  
Alessandra Altomonte ◽  
Claudio Cortes ◽  
Marchesa Bilio ◽  
Robert G Kelly ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cultured Cells ◽  
Time Window ◽  
Outflow Tract ◽  
Mouse Embryos ◽  
Cell Interactions ◽  
Deletion Syndrome ◽  
Cardiac Progenitors ◽  
Second Heart Field ◽  
Heart Field

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.

scholarly journals The role of secondary heart field in cardiac development

2009 ◽  
Vol 336 (2) ◽  
pp. 137-144 ◽  
Author(s):  
Laura A. Dyer ◽  
Margaret L. Kirby
Keyword(s):  
Cardiac Development ◽  
Heart Field ◽  
Secondary Heart Field

scholarly journals Hes1 Is Expressed in the Second Heart Field and Is Required for Outflow Tract Development

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