scholarly journals Tbx1 affects asymmetric cardiac morphogenesis by regulating Pitx2 in the secondary heart field

Development ◽  
2006 ◽  
Vol 133 (8) ◽  
pp. 1565-1573 ◽  
Author(s):  
S. Nowotschin
Keyword(s):  
Cardiac Morphogenesis ◽  
Heart Field ◽  
Secondary Heart Field

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 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 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 Tbx1 is regulated by forkhead proteins in the secondary heart field

2006 ◽  
Vol 235 (3) ◽  
pp. 701-710 ◽  
Author(s):  
Jun Maeda ◽  
Hiroyuki Yamagishi ◽  
John McAnally ◽  
Chihiro Yamagishi ◽  
Deepak Srivastava
Keyword(s):  
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

scholarly journals Vascular Smooth Muscle Cell Subpopulations and Neointimal Formation in Mouse Models of Elastin Insufficiency

2021 ◽  
Author(s):  
Chien-Jung Lin ◽  
Bridget Hunkins ◽  
Robyn Roth ◽  
Chieh-Yu Lin ◽  
Jessica E. Wagenseil ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Intimal Hyperplasia ◽  
Ascending Aorta ◽  
Specific Cell ◽  
Neointima Formation ◽  
Neointimal Formation ◽  
Internal Elastic Lamina ◽  
Heart Field ◽  
Secondary Heart Field ◽  
Elastic Lamina

Objective: Using a mouse model of Eln (elastin) insufficiency that spontaneously develops neointima in the ascending aorta, we sought to understand the origin and phenotypic heterogeneity of smooth muscle cells (SMCs) contributing to intimal hyperplasia. We were also interested in exploring how vascular cells adapt to the absence of Eln. Approach and Results: We used single-cell sequencing together with lineage-specific cell labeling to identify neointimal cell populations in a noninjury, genetic model of neointimal formation. Inactivating Eln production in vascular SMCs results in rapid intimal hyperplasia around breaks in the ascending aorta’s internal elastic lamina. Using lineage-specific Cre drivers to both lineage mark and inactivate Eln expression in the secondary heart field and neural crest aortic SMCs, we found that cells with a secondary heart field lineage are significant contributors to neointima formation. We also identified a small population of secondary heart field-derived SMCs underneath and adjacent to the internal elastic lamina. Within the neointima of SMC-Eln knockout mice, 2 unique SMC populations were identified that are transcriptionally different from other SMCs. While these cells had a distinct gene signature, they expressed several genes identified in other studies of neointimal lesions, suggesting that some mechanisms underlying neointima formation in Eln insufficiency are shared with adult vessel injury models. Conclusions: These results highlight the unique developmental origin and transcriptional signature of cells contributing to neointima in the ascending aorta. Our findings also show that the absence of Eln, or changes in elastic fiber integrity, influences the SMC biological niche in ways that lead to altered cell phenotypes.

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.

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