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The cardiac neural crest complex plays a vital role in forming connective tissues that aid in outflow septation and modelling of the aortic arch arteries during early development.<ref name="pmid20890117" /> Ablation of the complex often leads to impaired myocardial functioning similar to symptoms present in [[DiGeorge syndrome]].<ref name="pmid17224285">{{Cite journal |vauthors=Hutson MR, Kirby ML |date=2007 |title=Model systems for the study of heart development and disease: cardiac neural crest and conotruncal malformations |journal=Seminars in Cell & Developmental Biology |volume=18 |issue=1 |pages=101–110 |doi=10.1016/j.semcdb.2006.12.004 |pmc=1858673 |pmid=17224285}}</ref> Consequently, the removal of cardiac crest cells that populate in pharyngeal arches has flow on effects on the [[thymus]], [[parathyroid]] and [[thyroid gland]].<ref name="pmid1185098">{{Cite journal |vauthors=Le Lièvre CS, Le Douarin NM |date=1975 |title=Mesenchymal derivatives of the neural crest: analysis of chimaeric quail and chick embryos |journal=Development |volume=34 |issue=1 |pages=124–154 |pmid=1185098}}</ref>
[[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="Kirby (1987)">{{Cite journal |last=Kirby |first=Margaret L |year=1987 |title=Cardiac Morphogenesis—Recent Research Advances |url=https://www.nature.com/articles/pr198744.pdf |journal=Pediatric Research |publisher=Springer Science and Business Media LLC |volume=21 |issue=3 |pages=219–224 |doi=10.1203/00006450-198703000-00001 |pmid=3562119 |issn=0031-3998 |doi-access=free}}</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="Kirby (1987)" /><ref name="Gilbert (2010)">{{Cite book |last=Gilbert |first=S. F. |title=Developmental biology |publisher=Sinauer Associates |year=2010 |isbn=978-0-87893-243-
Cardiac neural crest cells (CNCCs) are a type of neural crest cells that migrate to the circumpharyngeal ridge (an arc-shape ridge above the [[pharyngeal arch]]es) and then into the 3rd, 4th and 6th pharyngeal arches and the cardiac outflow tract (OFT).<ref name="Kirby (1987)" /><ref name="Gilbert (2010)" /><ref name="Kuratani (1992)">{{Cite journal |
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="Kirby (1987)" /><ref name="Gilbert (2010)" />
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=== Induction ===
[[Neural induction]] is the differentiation of progenitor cells into their final designation or type. The progenitor cells which will become CNCCs are found in the [[epiblast]] about [[Primitive knot|Henson's node]].<ref name="Kuratani (1992)" /><ref name="Kirby (2010)">{{Cite journal |
=== Initial migration ===
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Many signaling molecules are required for the differentiation, proliferation, migration and [[apoptosis]] of the CNCCs. The molecular pathways involved include the [[Wnt signaling pathway|Wnt]], [[Notch signaling pathway|Notch]], [[Bone Morphogenetic Protein|BMP]], [[FGF8]] and [[GATA transcription factor|GATA]] families of molecules. In addition to these signaling pathways, these processes are also mediated by environmental factors including blood flow, shear stress, and blood pressure.<ref name="Niessen (2008)" />
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]]. The CNCCs themselves are the precursors to vascular smooth muscle cells and cardiac neurons.<ref name="Brown (2006)">{{Cite book |
For example, CNCCs are required for the formation of the [[aorticopulmonary septum]] (APS) that directs cardiac outflow into two tracts: the pulmonary trunk and the aorta of the developing heart. This is an example of [[remodelling]] which is dependent on signalling back and forth between CNCCs and the [[cardiogenic]] [[mesoderm]]. If this signalling is disrupted or there are defects in the CNCCS, cardiovascular anomalies may develop. These anomalies include [[persistent truncus arteriosus]] (PTA), [[double outlet right ventricle]] (DORV), [[tetralogy of Fallot]] and [[DiGeorge syndrome]].<ref name="Pompa (2012)">{{Cite journal |
=== Wnt ===
Wnt proteins are extracellular [[growth factor]]s that activate intracellular signalling pathways. There are two types of pathways: canonical and non-canonical. The classic canonical Wnt pathway involves [[β-catenin]] protein as a signaling mediator. Wnt maintains β-catenin by preventing against [[Proteasome]] degradation. Thus, β-catenin is stabilized in the presence of Wnt and regulates gene transcription through interaction with TCF/LEF transcription factors.<ref name="Gessert (2010)">{{Cite journal |
Wnt signaling pathways play a role in CNCC development as well as OFT development.<ref name="Gessert (2010)" /> In mice, decrease of β-catenin results in a decrease in the proliferation of CNCCs.<ref name="Gessert (2010)" /> Downregulation of the Wnt coreceptor [[Lrp6]] leads to a reduction of CNCCs in the dorsal neural tube and in the pharyngeal arches, and results in ventricular, septal, and OFT defects.<ref name="Gessert (2010)" /> Canonical Wnt signaling is especially important for cell cycle regulation of CNCC development and the initiation of CNCC migration.<ref name="Gessert (2010)" /> Non-canonical Wnt signaling plays a greater role in promoting cardiac differentiation and OFT development.<ref name="Gessert (2010)" />
=== Notch ===
[[Notch proteins|Notch]] is a transmembrane protein whose signaling is required for differentiation of CNCCs to vascular [[smooth muscle]] cells and for proliferation of cardiac [[myocytes]] (muscle cells of the heart). In mice, disruption of Notch signaling results in aortic arch branching defects and pulmonary stenosis, as well as a defect in the development of the smooth muscle cells of the sixth aortic arch artery, which is the precursor to the pulmonary artery.<ref name="Niessen (2008)">{{Cite journal |
=== Bone morphogenetic proteins ===
[[Bone morphogenetic protein]]s (BMPs) are required for neural crest cell migration into the cardiac cushions (precursors to heart valves and septa) and for differentiation of neural crest cells to smooth muscle cells of the aortic arch arteries. In neural crest–specific Alk2-deficient embryos, the cardiac cushions of the outflow tract are deficient in cells because of defects in neural crest cell migration.<ref name="Kaartinen (2004)">{{Cite journal |
=== Fibroblast growth factor 8 ===
[[Fibroblast growth factor 8]] (FGF8) transcription factors are essential for regulating the addition of secondary heart field cells into the cardiac outflow tract. FGF8 mouse mutants have a range of cardiac defects including underdeveloped arch arteries and transposition of the great arteries.<ref name="Abu-Issa (2002)">{{Cite journal |
=== GATA ===
[[GATA transcription factor]]s, which are complex molecules that bind to the DNA sequence ''GATA'', play a critical role in cell lineage differentiation restriction during cardiac development. The primary function of [[GATA6]] in cardiovascular development is to regulate the morphogenetic patterning of the outflow tract and aortic arch. When [[GATA6]] is inactivated in CNCCs, various cardiovascular defects such as persistent truncus arteriosus and interrupted aortic arch may occur. This phenotype (anomaly) was also observed when GATA6 was inactivated within vascular smooth muscle cells.<ref name="Lepore (2006)">{{Cite journal |last=Lepore |first=J. J. |date=2006-03-23 |title=GATA-6 regulates semaphorin 3C and is required in cardiac neural crest for cardiovascular morphogenesis |url=http://www.jci.org/articles/view/27363/files/pdf |journal=Journal of Clinical Investigation |volume=116 |issue=4 |pages=929–939 |doi=10.1172/JCI27363 |issn=0021-9738 |pmc=1409743 |pmid=16557299 |doi-access=free}}</ref> GATA6 in combination with Wnt (Wnt2-GATA6) plays a role in the development of the posterior pole of the heart (the inflow tract).<ref name="Tian (2010)">{{Cite journal |
== CNCCS and ischaemic heart disease ==
There is interest amongst researchers as to whether CNCCs can be used to repair human heart tissue. [[Myocardial infarction|Heart attacks]] in humans are common and their rate of mortality is high. There are emergency treatments that hospitals can administer, such as [[angioplasty]] or [[surgery]], but after that patients will likely be on medication for the long term and are more susceptible to heart attacks in the future. Other complications of heart attacks include [[cardiac arrhythmia]]s and [[heart failure]].<ref name="Canada (2012)">{{Cite web |title=Statistics |url=http://www.heartandstroke.com/site/c.ikIQLcMWJtE/b.3483991/k.34A8/Statistics.htm |archive-url=https://web.archive.org/web/20130104212608/http://www.heartandstroke.com/site/c.ikIQLcMWJtE/b.3483991/k.34A8/Statistics.htm |archive-date=2013-01-04 |website=Heart and Stroke Foundation of Canada}}</ref>
Although CNCCs are important in embryos, some CNCCs are retained in a dormant state to adulthood where they are called ''[[neural crest]] [[stem cells]]''. In 2005, Tomita transplanted neural crest stem cells from mammal hearts to the neural crest of chick embryos. These CNCCs were shown to migrate into the developing heart of the chick using the same dorsolateral pathway as the CNCCs, and differentiate into neural and glial cells.<ref name="Tomita (2005)">{{Cite journal |
Tamura's study of 2011 examined the fate of CNCCs after a heart attack (myocardial infarction) in young mice. The CNCCs in the young mice were tagged with enhanced [[green fluorescent protein]] (EGFP) and then traced. Tagged CNCCs were concentrated in the cardiac outflow tract, and some were found in the ventricular myocardium. These cells were also shown to be differentiating into cardiomyocytes as the heart grew. Although less were found, these EGFP-labelled CNCCs were still present in the adult heart. When a heart attack was induced, the CNCCs aggregated in the ischemic border zone area (an area of damaged tissue that can still be saved) and helped contribute to the regeneration of the tissue to some extent via differentiation into cardiomyocytes to replace the necrotic tissue.<ref name="Tamura (2011)">{{Cite journal |
== References ==
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