Cardiac neural crest: Difference between revisions

Revision as of 01:46, 10 September 2023

Revision as of 00:36, 30 November 2023

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The cardiac neural crest originates from the region of cells between somite 3 and the midotic placode that migrate towards and into the cardiac outflow tract.<ref name= "pmid2197017" >{{cite journal |vauthors= Le Lièvre CS, Le Douarin NM| title = Role of neural crest in congenital heart disease | journal = Circulation | volume = 82 | issue = 2 | pages = 332–340| date = 1990 | pmid = 2197017| doi = 10.1161/01.CIR.82.2.332 | doi-access = free }}</ref>

The cells migrate from the neural tube to populate pharyngeal arches 3, 4 and 6 with the largest population of the outflow tract originating from those in pharyngeal arches 4.<ref name="pmid20890117"/>

From here, a subpopulation of cells will develop into the endothelium of the [[aortic arch]] arteries while others will migrate into the outflow tract to form the aorticopulmonary and truncal septa.<ref name="pmid20890117"/><ref name= "pmid18005956" >{{cite journal |vauthors= Bajolle F, Zaffran S, Meilhac SM, Dandonneau M, Chang T, Kelly RG| title = Myocardium at the base of the aorta and pulmonary trunk is prefigured in the outflow tract of the heart and in subdomains of the second heart field | journal = Developmental Biology | volume = 313 | issue = 1 | pages = 25–34| date = 2008 | pmid = 18005956| doi = 10.1016/j.ydbio.2007.09.023 | doi-access = free }}</ref> Other ectomesenchymal cells will form the thymus and parathyroid glands.<ref name= "pmid6606851" >{{cite journal |vauthors= Bockman DE, Kirby ML| title = Dependence of thymus development on derivatives of the neural crest | journal = Science| volume = 223| issue =4635 | pages = 498–500| date = 1984| pmid = 6606851| doi = 10.1126/science.6606851 | bibcode = 1984Sci...223..498B }}</ref>

===Epithelial-mesenchymal transition===

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===Early migration===

During migration, crest cells destined for pharyngeal arches maintain contact with each other via [[lamellipodia]] and [[filopodia]]. Short range local contact is maintained with lamellipodia whilst long range non-local contact is maintained with filopodia.<ref name="pmid15548586”">{{cite journal |vauthors= Teddy JM, Kulesa PM| title = In vivo evidence for short-and long-range cell communication in cranial neural crest cells | journal = Development| volume = 131| issue=24 | pages =6141–6151| date = 2004| pmid = 15548586| doi = 10.1242/dev.01534 | doi-access = free}}</ref> During this process, [[connexin 43]] (Cx43) regulates cell interaction by regulating the formation of channels known as [[gap junctions]].<ref name="pmid17619792"/> Impaired Cx43 function in transgenic mice leads to altered coronary artery patterns and abnormal outflow tracts.<ref name= "pmid9640330" >{{cite journal |vauthors= Huang GY, Wessels A, Smith BR, Linask KK, Ewart JL, Lo CW| title = Alteration in connexin 43 gap junction gene dosage impairs conotruncal heart development | journal = Developmental Biology| volume = 198| issue = 1 | pages = 32–44| date = 1998| pmid = 9640330| doi = 10.1006/dbio.1998.8891 | doi-access = free}}</ref> Further gap junction signalling is dependent on a [[cadherin]] mediated cell adhesion formed during cross talking with p120 catenin signalling.<ref name= "pmid11449002" >{{cite journal |vauthors= Xu X, Li WE, Huang GY, Meyer R, Chen T, Luo Y, Thomas MP, Radice GL, Lo CW | title = Modulation of mouse neural crest cell motility by N-cadherin and connexin 43 gap junctions | journal = Journal of Cell Biology| volume = 154 | issue = 1 | pages = 217–230| date = 2001| pmid= 11449002| pmc = 2196865 | doi = 10.1083/jcb.200105047 }}</ref>

Appropriate outflow tract formation relies on a [[morphogen]] concentration gradient set up by [[fibroblast growth factor]] (FGF) secreting cells. Cardiac crest cells furthest away from FGF secreting cells will receive lower concentrations of FGF8 signalling than cells closer to FGF secreting cells. This allows for appropriate formation of the outflow tract.<ref name= "pmid12223417" >{{cite journal |vauthors= Abu-Issa R, Smyth G, Smoak I, Yamamura K, Meyers EN | title = Fgf8 is required for pharyngeal arch and cardiovascular development in the mouse | journal = Development| volume = 129| issue = 19 | pages = 4613–4625| date = 2002| doi = 10.1242/dev.129.19.4613 | pmid = 12223417}}</ref> Cells located in rhombomeres 3and 5 undergo programmed cell death under signalling cues from [[semaphorins]]. The lack of cells in this region results in the formation of crest-free zones.<ref name= "pmmid18625214" >{{cite journal| vauthors= Toyofuku T, Yoshida J, Sugimoto T, Yamamoto M, Makino N, Takamatsu H, Takegahara N, Suto F, Hori M, Fujisawa H, Kumanogoh A, Kukutani H| title = Repulsive and attractive semaphorins cooperate to direct the navigation of cardiac neural crest cells | journal = The Scientific World Journal| volume = 7 | issue = 1 | pages = 1090–1113| date = 2007| pmid = 18625214| doi = 10.1016/j.ydbio.2008.06.028 | doi-access = free}}</ref>

The process of migration requires a permissive extracellular matrix.<ref name="pmid20890117"/> The [[enzyme]] [[arginyltransferase]] creates this environment by adding an arginyl group onto newly synthesised proteins during [[post-translational modification]].<ref name= "pmid20300656" >{{cite journal| vauthors= Kurosaka S, Leu NA, Zhang F, Bunte R, Saha S, Wang J, Guo C, He W, Kashina A| title = Arginylation-dependent neural crest cell migration is essential for mouse development. | journal = PLOS Genetics| volume = 6| issue =3 | pages = e1000878| date = 2010| pmid =20300656| pmc = 2837401 | doi = 10.1371/journal.pgen.1000878 | doi-access = free }}</ref> This process aids cells motility and ensures the proteins contained within the actin cytoskeleton is prepped for migration.<ref name="pmid20890117"/>