Cardiac neural crest: Difference between revisions

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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 [[Pharyngealpharyngeal arch|pharyngeal arches]]es) and then into the 3rd, 4th and 6th pharyngeal arches and the cardiac outflow tract (OFT).<ref name="kirby1987" /><ref name="gilbert" /><ref name= "kur">{{cite journal|last=Kuratani|first=S.C.|coauthors=Kirby, M.L.|title=Migration and distribution of circumpharyngeal crest cells in the chick embryo. Formation of the circumpharyngeal ridge and E/C8+ crest cells in the vertebrate head region|journal=Anat. Rec.|year=1992|month=Oct|volume=234|issue=2|pages=263–268|pmid=1384396|doi=10.1002/ar.1092340213}}</ref> They extend from the [[otic placode]]s (the structure in developing embryos that will later form the ears) to the third [[somite]]s (clusters of [[mesoderm]] that will become skeletal muscle, vertebrae and dermis).<ref name="kirby1987" /><ref name="gilbert" />
 
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 [[ GATA transcription factor|GATA]] families. In addition to these signaling pathways, these processes are also mediated by environmental factors including blood flow, shear stress, and blood pressure.<ref name=Niessen2008 />
 
=== 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|year= April 2006|month=April|volume=116|issue=4|pages=929–939|doi=10.1172/JCI27363|url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1409743/pdf/JCI0627363.pdf|accessdate=November 19, 2012|pmid=16557299|pmc=1409743}}</ref> Therefore the primary function of GATA-6 in cardiovascular development is to regulate the morphogenetic patterning of the outflow tract and aortic arch. It is also found that GATA6-Wnt2 also play a role in the development of the posterior pole of the heart (inflow tract).<ref name=Tian2010>{{cite journal|last=Tian|first=Ying|coauthors=Yuan, LJ, Goss, AM, Wang, T, Yang, J, Lepore, JJ, Zhou, D, Schwartz, RJ, Patel, V., Cohen, ED, & Morrisey, EE|title=Characterization and In Vivo Pharmacological Rescue of a Wnt2-Gata6 Pathway Required for Cardiac Inflow Tract Development|journal=Developmental Cell|date=16|year= February 2010|month=February|volume=18|issue=2|pages=275–287|url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846539/pdf/nihms177061.pdf|accessdate=November 19, 2012|pmc=2846539|pmid=20159597|doi=10.1016/j.devcel.2010.01.008}}</ref>
 
==Regenerative Medicine==