Talk:Neural Crest - Cardiac
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Cite this page: Hill, M.A. (2019, July 16) Embryology Neural Crest - Cardiac. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Neural_Crest_-_Cardiac
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Cardiac Neural Crest
<pubmed limit=5>Cardiac Neural Crest</pubmed>
Foxc2 is required for proper cardiac neural crest cell migration, outflow tract septation, and ventricle expansion
Dev Dyn. 2018 Dec;247(12):1286-1296. doi: 10.1002/dvdy.24684.
Inman KE1, Caiaffa CD2, Melton KR3, Sandell LL4, Achilleos A5, Kume T6, Trainor PA2,7.
Abstract BACKGROUND: Proper development of the great vessels of the heart and septation of the cardiac outflow tract requires cardiac neural crest cells. These cells give rise to the parasympathetic cardiac ganglia, the smooth muscle layer of the great vessels, some cardiomyocytes, and the conotruncal cushions and aorticopulmonary septum of the outflow tract. Ablation of cardiac neural crest cells results in defective patterning of each of these structures. Previous studies have shown that targeted deletion of the forkhead transcription factor C2 (Foxc2), results in cardiac phenotypes similar to that derived from cardiac neural crest cell ablation. RESULTS: We report that Foxc2-/- embryos on the 129s6/SvEv inbred genetic background display persistent truncus arteriosus and hypoplastic ventricles before embryonic lethality. Foxc2 loss-of-function resulted in perturbed cardiac neural crest cell migration and their reduced contribution to the outflow tract as evidenced by lineage tracing analyses together with perturbed expression of the neural crest cell markers Sox10 and Crabp1. Foxc2 loss-of-function also resulted in alterations in PlexinD1, Twist1, PECAM1, and Hand1/2 expression in association with vascular and ventricular defects. CONCLUSIONS: Our data indicate Foxc2 is required for proper migration of cardiac neural crest cells, septation of the outflow tract, and development of the ventricles. Developmental Dynamics 247:1286-1296, 2018. © 2018 Wiley Periodicals, Inc. © 2018 Wiley Periodicals, Inc.
KEYWORDS: Foxc2; cardiac neural crest; common arterial trunk; heart development; outflow tract; persistent truncus arteriosus PMID: 30376688 PMCID: PMC6275097 [Available on 2019-12-01] DOI: 10.1002/dvdy.24684
Development of the Human Aortic Arch System Captured in an Interactive Three-Dimensional Reference Model
Am J Med Genet A. 2013 Apr 23. doi: 10.1002/ajmg.a.35881. [Epub ahead of print]
Rana MS, Sizarov A, Christoffels VM, Moorman AF. Source Heart Failure Research Center, Department of Anatomy, Embryology and Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Variations and mutations in the human genome, such as 22q11.2 microdeletion, can increase the risk for congenital defects, including aortic arch malformations. Animal models are increasingly expanding our molecular and genetic insights into aortic arch development. However, in order to justify animal-to-human extrapolations, a human morphological, and molecular reference model would be of great value, but is currently lacking. Here, we present interactive three-dimensional reconstructions of the developing human aortic arch system, supplemented with the protein distribution of developmental markers for patterning and growth, including T-box transcription factor TBX1, a major candidate for the phenotypes found in patients with the 22q11.2 microdeletion. These reconstructions and expression data facilitate unbiased interpretations, and reveal previously unappreciated aspects of human aortic arch development. Based on our reconstructions and on reported congenital anomalies of the pulmonary trunk and tributaries, we postulate that the pulmonary arteries originate from the aortic sac, rather than from the sixth pharyngeal arch arteries. Similar to mouse, TBX1 is expressed in pharyngeal mesenchyme and epithelia. The endothelium of the pharyngeal arch arteries is largely negative for TBX1 and family member TBX2 but expresses neural crest marker AP2α, which gradually decreases with ongoing development of vascular smooth muscle. At early stages, the pharyngeal arch arteries, aortic sac, and the dorsal aortae in particular were largely negative for proliferation marker Ki67, potentially an important parameter during aortic arch system remodeling. Together, our data support current animal-to-human extrapolations and future genetic and molecular analyses using animal models of congenital heart disease. © 2013 Wiley Periodicals, Inc. Copyright © 2013 Wiley Periodicals, Inc.
FGF8 signaling is chemotactic for cardiac neural crest cells
Dev Biol. 2011 Jun 1;354(1):18-30. doi: 10.1016/j.ydbio.2011.03.010. Epub 2011 Mar 17.
Sato A, Scholl AM, Kuhn EN, Stadt HA, Decker JR, Pegram K, Hutson MR, Kirby ML. Source Department of Pediatrics (Neonatology), Duke University, Durham, NC 27710, USA. Erratum in Dev Biol. 2012 Oct 1;370(1):164. Kuhn, E B [corrected to Kuhn, E N]. Abstract Cardiac neural crest cells migrate into the pharyngeal arches where they support development of the pharyngeal arch arteries. The pharyngeal endoderm and ectoderm both express high levels of FGF8. We hypothesized that FGF8 is chemotactic for cardiac crest cells. To begin testing this hypothesis, cardiac crest was explanted for migration assays under various conditions. Cardiac neural crest cells migrated more in response to FGF8. Single cell tracing indicated that this was not due to proliferation and subsequent transwell assays showed that the cells migrate toward an FGF8 source. The migratory response was mediated by FGF receptors (FGFR) 1 and 3 and MAPK/ERK intracellular signaling. To test whether FGF8 is chemokinetic and/or chemotactic in vivo, dominant negative FGFR1 was electroporated into the premigratory cardiac neural crest. Cells expressing the dominant negative receptor migrated slower than normal cardiac neural crest cells and were prone to remain in the vicinity of the neural tube and die. Treating with the FGFR1 inhibitor, SU5402 or an FGFR3 function-blocking antibody also slowed neural crest migration. FGF8 over-signaling enhanced neural crest migration. Neural crest cells migrated to an FGF8-soaked bead placed dorsal to the pharynx. Finally, an FGF8 producing plasmid was electroporated into an ectopic site in the ventral pharyngeal endoderm. The FGF8 producing cells attracted a thick layer of mesenchymal cells. DiI labeling of the neural crest as well as quail-to-chick neural crest chimeras showed that neural crest cells migrated to and around the ectopic site of FGF8 expression. These results showing that FGF8 is chemotactic and chemokinetic for cardiac neural crest adds another dimension to understanding the relationship of FGF8 and cardiac neural crest in cardiovascular defects. Copyright © 2011 Elsevier Inc. All rights reserved.
Factors controlling cardiac neural crest cell migration
Cell Adh Migr. 2010 Oct-Dec;4(4):609-21.
Kirby ML, Hutson MR. Source Department of Pediatrics, Duke University, Durham, NC, USA. firstname.lastname@example.org Abstract Cardiac neural crest cells originate as part of the postotic caudal rhombencephalic neural crest stream. Ectomesenchymal cells in this stream migrate to the circumpharyngeal ridge and then into the caudal pharyngeal arches where they condense to form first a sheath and then the smooth muscle tunics of the persisting pharyngeal arch arteries. A subset of the cells continue migrating into the cardiac outflow tract where they will condense to form the aorticopulmonary septum. Cell signaling, extracellular matrix and cell-cell contacts are all critical for the initial migration, pauses, continued migration, and condensation of these cells. This review elucidates what is currently known about these factors. PMID 20890117