scholarly journals Vangl2-Regulated Polarisation of Second Heart Field-Derived Cells Is Required for Outflow Tract Lengthening during Cardiac Development

PLoS Genetics ◽  
2014 ◽  
Vol 10 (12) ◽  
pp. e1004871 ◽  
Author(s):  
Simon A. Ramsbottom ◽  
Vipul Sharma ◽  
Hong Jun Rhee ◽  
Lorraine Eley ◽  
Helen M. Phillips ◽  
...  
Keyword(s):  
Cardiac Development ◽  
Outflow Tract ◽  
Second Heart Field ◽  
Heart Field

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 Lamb1a regulates atrial growth by limiting excessive, contractility-dependent second heart field addition during zebrafish heart development

2021 ◽  
Author(s):  
Christopher J. Derrick ◽  
Eric J. G. Pollitt ◽  
Ashley Sanchez Sevilla Uruchurtu ◽  
Farah Hussein ◽  
Emily S. Noёl
Keyword(s):  
Heart Development ◽  
Cardiac Development ◽  
Basement Membranes ◽  
Atrioventricular Canal ◽  
Cardiac Morphogenesis ◽  
Heart Morphogenesis ◽  
Second Heart Field ◽  
Heart Field ◽  
Heart Size ◽  
Zebrafish Heart

AbstractDuring early vertebrate heart development, the heart transitions from a linear tube to a complex asymmetric structure. This process includes looping of the tube and ballooning of the emerging cardiac chambers, which occur simultaneously with growth of the heart. A key driver of cardiac growth is deployment of cells from the Second Heart Field (SHF) into both poles of the heart, with cardiac morphogenesis and growth intimately linked in heart development. Laminin is a core component of extracellular matrix (ECM) basement membranes, and although mutations in specific laminin subunits are linked with a variety of cardiac abnormalities, including congenital heart disease and dilated cardiomyopathy, no role for laminin has been identified in early vertebrate heart morphogenesis. We identified dynamic, tissue-specific expression of laminin subunit genes in the developing zebrafish heart, supporting a role for laminins in heart morphogenesis.lamb1amutants exhibit cardiomegaly from 2dpf onwards, with subsequent progressive defects in cardiac morphogenesis characterised by a failure of the chambers to compact around the developing atrioventricular canal. We show that loss oflamb1aresults in excess addition of SHF cells to the atrium, revealing that Lamb1a functions to limit heart size during cardiac development by restricting SHF addition to the venous pole.lamb1amutants exhibit hallmarks of altered haemodynamics, and specifically blocking cardiac contractility inlamb1amutants rescues heart size and atrial SHF addition. Furthermore, we identify that FGF and RA signalling, two conserved pathways promoting SHF addition, are regulated by heart contractility and are dysregulated inlamb1amutants, suggesting that laminin mediates interactions between SHF deployment, heart biomechanics, and biochemical signalling during heart development. Together, this describes the first requirement for laminins in early vertebrate heart morphogenesis, reinforcing the importance of specialised ECM composition in cardiac development.

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 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

scholarly journals Myocardium at the base of the aorta and pulmonary trunk is prefigured in the outflow tract of the heart and in subdomains of the second heart field

2008 ◽  
Vol 313 (1) ◽  
pp. 25-34 ◽  
Author(s):  
Fanny Bajolle ◽  
Stéphane Zaffran ◽  
Sigolène M. Meilhac ◽  
Mathieu Dandonneau ◽  
Ted Chang ◽  
...  
Keyword(s):  
Outflow Tract ◽  
Pulmonary Trunk ◽  
Second Heart Field ◽  
Heart Field

scholarly journals Isl1 Expression at the Venous Pole Identifies a Novel Role for the Second Heart Field in Cardiac Development

2007 ◽  
Vol 101 (10) ◽  
pp. 971-974 ◽  
Author(s):  
Brian S. Snarr ◽  
Jessica L. O’Neal ◽  
Mastan R. Chintalapudi ◽  
Elaine E. Wirrig ◽  
Aimee L. Phelps ◽  
...  
Keyword(s):  
Cardiac Development ◽  
Second Heart Field ◽  
Heart Field

scholarly journals Regulation of Sema3c and the Interaction between Cardiac Neural Crest and Second Heart Field during Outflow Tract Development

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Kazuki Kodo ◽  
Shinsuke Shibata ◽  
Sachiko Miyagawa-Tomita ◽  
Sang-Ging Ong ◽  
Hiroshi Takahashi ◽  
...  
Keyword(s):  
Neural Crest ◽  
Outflow Tract ◽  
Cardiac Neural Crest ◽  
Second Heart Field ◽  
Heart Field

scholarly journals Lamb1a regulates atrial growth by limiting second heart field addition during zebrafish heart development

Development ◽  
2021 ◽  
Author(s):  
Christopher J. Derrick ◽  
Eric J. G. Pollitt ◽  
Ashley Sanchez Sevilla Uruchurtu ◽  
Farah Hussein ◽  
Andrew J. Grierson ◽  
...  
Keyword(s):  
Heart Development ◽  
Cardiac Development ◽  
Cardiac Contractility ◽  
Asymmetric Structure ◽  
Specific Expression ◽  
Heart Morphogenesis ◽  
Second Heart Field ◽  
Heart Field ◽  
Heart Size ◽  
Zebrafish Heart

During early vertebrate heart development the heart transitions from a linear tube to a complex asymmetric structure, a morphogenetic process which occurs simultaneously with growth of the heart. Cardiac growth during early heart morphogenesis is driven by deployment of cells from the Second Heart Field (SHF) into both poles of the heart. Laminin is a core component of the extracellular matrix (ECM), and although mutations in laminin subunits are linked with cardiac abnormalities, no role for laminin has been identified in early vertebrate heart morphogenesis. We identified tissue-specific expression of laminin genes in the developing zebrafish heart, supporting a role for laminins in heart morphogenesis. Analysis of heart development in lamb1a zebrafish mutant embryos reveals mild morphogenetic defects and progressive cardiomegaly, and that Lamb1a functions to limit heart size during cardiac development by restricting SHF addition. lamb1a mutants exhibit hallmarks of altered haemodynamics, and blocking cardiac contractility in lamb1a mutants rescues heart size and atrial SHF addition. Together this suggests that laminin mediates interactions between SHF deployment and cardiac biomechanics during heart development and growth in the developing embryo.

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