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 Cardiac neural crest is necessary for normal addition of the myocardium to the arterial pole from the secondary heart field

2005 ◽  
Vol 281 (1) ◽  
pp. 66-77 ◽  
Author(s):  
Karen L. Waldo ◽  
Mary R. Hutson ◽  
Harriett A. Stadt ◽  
Marzena Zdanowicz ◽  
Jaroslaw Zdanowicz ◽  
...  
Keyword(s):  
Neural Crest ◽  
Cardiac Neural Crest ◽  
Heart Field ◽  
Secondary 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 Foxc2 is required for proper cardiac neural crest cell migration, outflow tract septation, and ventricle expansion

2018 ◽  
Vol 247 (12) ◽  
pp. 1286-1296 ◽  
Author(s):  
Kimberly E. Inman ◽  
Carlo Donato Caiaffa ◽  
Kristin R. Melton ◽  
Lisa L. Sandell ◽  
Annita Achilleos ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Outflow Tract ◽  
Cardiac Neural Crest ◽  
Neural Crest Cell Migration ◽  
Crest Cell

Pax3 is required for cardiac neural crest migration in the mouse: evidence from the splotch (Sp2H) mutant

Development ◽  
1997 ◽  
Vol 124 (2) ◽  
pp. 505-514 ◽  
Author(s):  
S.J. Conway ◽  
D.J. Henderson ◽  
A.J. Copp
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Outflow Tract ◽  
Avian Embryo ◽  
Cardiac Neural Crest ◽  
Branchial Arches ◽  
Aortic Arches ◽  
Cardiac Outflow

Neural crest cells originating in the occipital region of the avian embryo are known to play a vital role in formation of the septum of the cardiac outflow tract and to contribute cells to the aortic arches, thymus, thyroid and parathyroids. This ‘cardiac’ neural crest sub-population is assumed to exist in mammals, but without direct evidence. In this paper we demonstrate, using RT-PCR and in situ hybridisation, that Pax3 expression can serve as a marker of cardiac neural crest cells in the mouse embryo. Cells of this lineage were traced from the occipital neural tube, via branchial arches 3, 4 and 6, into the aortic sac and aorto-pulmonary outflow tract. Confirmation that these Pax3-positive cells are indeed cardiac neural crest is provided by experiments in which hearts were deprived of a source of colonising neural crest, by organ culture in vitro, with consequent lack of up-regulation of Pax3. Occipital neural crest cell outgrowths in vitro were also shown to express Pax3. Mutation of Pax3, as occurs in the splotch (Sp2H) mouse, results in development of conotruncal heart defects including persistent truncus arteriosus. Homozygotes also exhibit defects of the aortic arches, thymus, thyroid and parathyroids. Pax3-positive neural crest cells were found to emigrate from the occipital neural tube of Sp2H/Sp2H embryos in a relatively normal fashion, but there was a marked deficiency or absence of neural crest cells traversing branchial arches 3, 4 and 6, and entering the cardiac outflow tract. This decreased expression of Pax3 in Sp2H/Sp2H embryos was not due to down-regulation of Pax3 in neural crest cells, as use of independent neural crest markers, Hoxa-3, CrabpI, Prx1, Prx2 and c-met also revealed a deficiency of migrating cardiac neural crest cells in homozygous embryos. This work demonstrates the essential role of the cardiac neural crest in formation of the heart and great vessels in the mouse and, furthermore, shows that Pax3 function is required for the cardiac neural crest to complete its migration to the developing heart.

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 Semaphorin3D regulates invasion of cardiac neural crest cells into the primary heart field

2006 ◽  
Vol 298 (1) ◽  
pp. 12-21 ◽  
Author(s):  
Mariko Sato ◽  
Huai-Jen Tsai ◽  
H. Joseph Yost
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Cardiac Neural Crest ◽  
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.

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