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[[Neural crest]] cells are a group of temporary, [[Cell potency#Multipotency|multipotent]] (can give rise to some other types of cells but not all) cells that are pinched off during the formation of the [[neural tube]] (precursor to the [[spinal cord]] and brain) and therefore are found at the dorsal (top) region of the neural tube during development.<ref name ="kirby1987">{{cite journal|last=Kirby|first=M|title=Cardiac Morphogenesis--Recent Research Advances|journal=Pediatric Research|year=1987|volume=21|issue=3|pages=219–224|url=http://www.nature.com/pr/journal/v21/n3/pdf/pr198744a.pdf}}</ref> They are derived from the [[ectoderm]] germ layer, but are sometimes called the fourth germ layer because they are so important and give rise to so many other types of cells.<ref name="kirby1987" /><ref name= "gilbert">{{cite book|last=Gilbert|first=S.F.|title=Developmental Biology|year=2010|publisher=Sinauer Associates|___location=MA|pages=373–389|url=http://www.ncbi.nlm.nih.gov/books/NBK10065/}}</ref> They migrate throughout the body and create a large number of differentiated cells such as [[neuron]]s, glial cells, pigment-containing cells in skin, skeletal tissue cells in the head, and many more.<ref name="kirby1987" /><ref name="gilbert" />
Cardiac neural crest cells (CNCCs) are a type of neural crest cells that migrate to the circumpharyngeal ridge (an arc-shape ridge above the [[
The cardiac neural crest cells:<ref name="kirby1987" /><ref name="gilbert" />
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The CNCCs are required for the formation of the [[aorticopulmonary septum]] (APS) that separates the cardiac outflow into the pulmonary trunk and the aorta in normal heart development. This remodeling of the OFT requires the reciprocal signaling between CNCCs and cardiogenic mesoderm. Cardiovascular dysfunction can result either from a disruption in this signaling or defects in cardiac neural crest cells. The CNCCs interact with the cardiogenic mesoderm cells of the primary and secondary heart fields, which are derived from the cardiac crescent and will give rise to the [[endocardium]], myocardium, and [[epicardium]].<ref name=Pompa2012>{{cite journal|last=de la Pompa|first=J.L.|coauthors=Epstein, JA|title=Coordination Tissue Interactions: Notch Signalling in Cardiac Development and Disease|journal=Developmental Cell|date=|year=2012|month=February|volume=22|issue=2|pages=244–264|doi=10.1016/j.devcel.2012.01.014|accessdate=November 19, 2012}}</ref> The CNCCs themselves are the precursors to vascular smooth muscle cells and cardiac neurons.<ref name=Brown2006>{{cite journal|last=Brown|first=Christopher|coauthors=Baldwin, H|title=Neural Crest Contribution to the Cardiovascular System|journal=Advances in Experimental Medicine|year=2006|volume=589|pages=134–154|doi=10.1007/978-0-387-46954-6_8|accessdate=November 19, 2012}}</ref> Common defects related to CNCCs can result in congenital heart malformations such as [[persistent truncus arteriosus]] (PTA), [[double outlet right ventricle]] (DORV), [[tetralogy of Fallot]] and [[DiGeorge syndrome]].
Many signaling molecules are required for the differentiation, proliferation, migration and [[apoptosis]] of the CNCCs. The major molecular pathways involve members of the [[Wnt signaling pathway|Wnt]], [[Notch signaling pathway|Notch]], [[Bone Morphogenetic Protein|BMP]], [[FGF8]] and [[
=== Wnt ===
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=== GATA ===
GATA transcription factors also play critical roles in cell lineage differentiation restriction during cardiac development. When GATA-6 is inactivated in the CNCCs it can lead to various cardiovascular defects such as persistent truncus arteriorus and interrupted aortic arch. This phenotype was also observed when GATA-6 was inactivated within the vascular smooth muscle cells (VSMCs).<ref name=Lepore2006>{{cite journal|last=Lepore|first=John J|coauthors=Mericko, PA, Cheng, L., Lu, MM, Morrisey, EE, & Parmacek, MS|title=GATA-6 regulates semaphorin 3C and is required in cardiac neural crest for cardiovascular morphogenesis|journal=Journnal of Clinical Investigation|date=3
==Regenerative Medicine==
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