Cardiac neural crest: Difference between revisions

Revision as of 07:56, 15 September 2021

Revision as of 21:06, 12 June 2022

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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 = PLoSPLOS Genetics| volume = 6| issue =3 | pages = e1000878| date = 2010| pmid =20300656| pmc = 2837401 | doi = 10.1371/journal.pgen.1000878 }}</ref> This process aids cells motility and ensures proteins the proteins contained within the actin cytoskeleton is prepped for migration.<ref name="pmid20890117"/>

===Circumpharyngeal ridge===

Cell migration towards the circumpharyngeal ridge is forced to paused to allow for the formation of the caudal pharyngeal arches.<ref name="pmid20890117"/> Little is known about this pausing mechanism, but studies conducted in chicks have uncovered the role of [[mesoderm]] expressed factors EphrinB3 and EphrinB4 in forming fibronectin attachments.<ref name= "pmid12117812" >{{cite journal |vauthors= Santiago A, Erickson CA | title = Ephrin-B ligands play a dual role in the control of neural crest cell migration | journal = Development| volume = 129| issue = 15 | pages = 3621–3623| date = 2002| doi = 10.1242/dev.129.15.3621 | pmid = 12117812}}</ref>

===Caudal pharynx and arch artery condensation===

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===Pulmonary venous system===

During [[cardiogenesis]], migration of the cardiac neural crest complex occurs prior to the development of the pulmonary system. There is no visible difference in the pulmonary veins of chick embryos that developed persistent truncus arteriosus and embryos with an intact cardiac neural crest complex. Ablation of the cardiac neural crest complex do not play a role in the systemic or pulmonary venous system as no visible venous defects is observed.<ref name= "pmid2923280" >{{cite journal |vauthors= Phillips III MT, Waldo K, Kirby ML| title = Neural crest ablation does not alter pulmonary vein development in the chick embryo. | journal = The Anatomical Record| volume = 223| issue =3 | pages = 292–298| date = 1989| pmid = 2923280| doi = 10.1002/ar.1092230308| s2cid = 11552278 }}</ref>

===Derivative development===

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==Location==

Into the [[pharyngeal arches]] and [[Truncus arteriosus (embryology)]], forming the [[aorticopulmonary septum]]<ref name="pmid10725237">{{cite journal |vauthors=Jiang X, Rowitch DH, Soriano P, McMahon AP, Sucov HM |title=Fate of the mammalian cardiac neural crest |journal=Development |volume=127 |issue=8 |pages=1607–16 |date=April 2000 |doi=10.1242/dev.127.8.1607 |pmid=10725237 |url=http://dev.biologists.org/cgi/pmidlookup?view=long&pmid=10725237}}</ref> and the [[smooth muscle]] of [[great arteries]].

Anterior of the aorta to become the four [[pre-aortic ganglia]]: ([[celiac ganglion]], [[superior mesenteric ganglion]], [[inferior mesenteric ganglion]] and [[aortical renal ganglia]]).