Neural Crest - Cardiac
|Embryology - 23 Aug 2017 Expand to Translate|
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- 1 Introduction
- 2 Some Recent Findings
- 3 2013
- 4 2011
- 5 2010
- 6 10 Most Recent
- 7 References
- 8 Glossary Links
Draft Page (notice removed when completed).
Cardiovascular System Development
Some Recent Findings
Development of the Human Aortic Arch System Captured in an Interactive Three-Dimensional Reference Model
Am J Med Genet A. 2013 Apr 23. doi: 10.1002/ajmg.a.35881. [Epub ahead of print]
Rana MS, Sizarov A, Christoffels VM, Moorman AF. Source Heart Failure Research Center, Department of Anatomy, Embryology and Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Variations and mutations in the human genome, such as 22q11.2 microdeletion, can increase the risk for congenital defects, including aortic arch malformations. Animal models are increasingly expanding our molecular and genetic insights into aortic arch development. However, in order to justify animal-to-human extrapolations, a human morphological, and molecular reference model would be of great value, but is currently lacking. Here, we present interactive three-dimensional reconstructions of the developing human aortic arch system, supplemented with the protein distribution of developmental markers for patterning and growth, including T-box transcription factor TBX1, a major candidate for the phenotypes found in patients with the 22q11.2 microdeletion. These reconstructions and expression data facilitate unbiased interpretations, and reveal previously unappreciated aspects of human aortic arch development. Based on our reconstructions and on reported congenital anomalies of the pulmonary trunk and tributaries, we postulate that the pulmonary arteries originate from the aortic sac, rather than from the sixth pharyngeal arch arteries. Similar to mouse, TBX1 is expressed in pharyngeal mesenchyme and epithelia. The endothelium of the pharyngeal arch arteries is largely negative for TBX1 and family member TBX2 but expresses neural crest marker AP2α, which gradually decreases with ongoing development of vascular smooth muscle. At early stages, the pharyngeal arch arteries, aortic sac, and the dorsal aortae in particular were largely negative for proliferation marker Ki67, potentially an important parameter during aortic arch system remodeling. Together, our data support current animal-to-human extrapolations and future genetic and molecular analyses using animal models of congenital heart disease. © 2013 Wiley Periodicals, Inc. Copyright © 2013 Wiley Periodicals, Inc.
FGF8 signaling is chemotactic for cardiac neural crest cells
Dev Biol. 2011 Jun 1;354(1):18-30. doi: 10.1016/j.ydbio.2011.03.010. Epub 2011 Mar 17.
Sato A, Scholl AM, Kuhn EN, Stadt HA, Decker JR, Pegram K, Hutson MR, Kirby ML. Source Department of Pediatrics (Neonatology), Duke University, Durham, NC 27710, USA. Erratum in Dev Biol. 2012 Oct 1;370(1):164. Kuhn, E B [corrected to Kuhn, E N]. Abstract Cardiac neural crest cells migrate into the pharyngeal arches where they support development of the pharyngeal arch arteries. The pharyngeal endoderm and ectoderm both express high levels of FGF8. We hypothesized that FGF8 is chemotactic for cardiac crest cells. To begin testing this hypothesis, cardiac crest was explanted for migration assays under various conditions. Cardiac neural crest cells migrated more in response to FGF8. Single cell tracing indicated that this was not due to proliferation and subsequent transwell assays showed that the cells migrate toward an FGF8 source. The migratory response was mediated by FGF receptors (FGFR) 1 and 3 and MAPK/ERK intracellular signaling. To test whether FGF8 is chemokinetic and/or chemotactic in vivo, dominant negative FGFR1 was electroporated into the premigratory cardiac neural crest. Cells expressing the dominant negative receptor migrated slower than normal cardiac neural crest cells and were prone to remain in the vicinity of the neural tube and die. Treating with the FGFR1 inhibitor, SU5402 or an FGFR3 function-blocking antibody also slowed neural crest migration. FGF8 over-signaling enhanced neural crest migration. Neural crest cells migrated to an FGF8-soaked bead placed dorsal to the pharynx. Finally, an FGF8 producing plasmid was electroporated into an ectopic site in the ventral pharyngeal endoderm. The FGF8 producing cells attracted a thick layer of mesenchymal cells. DiI labeling of the neural crest as well as quail-to-chick neural crest chimeras showed that neural crest cells migrated to and around the ectopic site of FGF8 expression. These results showing that FGF8 is chemotactic and chemokinetic for cardiac neural crest adds another dimension to understanding the relationship of FGF8 and cardiac neural crest in cardiovascular defects. Copyright © 2011 Elsevier Inc. All rights reserved.
Factors controlling cardiac neural crest cell migration
Cell Adh Migr. 2010 Oct-Dec;4(4):609-21.
Kirby ML, Hutson MR. Source Department of Pediatrics, Duke University, Durham, NC, USA. email@example.com Abstract Cardiac neural crest cells originate as part of the postotic caudal rhombencephalic neural crest stream. Ectomesenchymal cells in this stream migrate to the circumpharyngeal ridge and then into the caudal pharyngeal arches where they condense to form first a sheath and then the smooth muscle tunics of the persisting pharyngeal arch arteries. A subset of the cells continue migrating into the cardiac outflow tract where they will condense to form the aorticopulmonary septum. Cell signaling, extracellular matrix and cell-cell contacts are all critical for the initial migration, pauses, continued migration, and condensation of these cells. This review elucidates what is currently known about these factors. PMID 20890117
10 Most Recent
Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)
Cardiac Neural Crest
M Komiyama Cardio-cephalic neural crest syndrome: A novel hypothesis of vascular neurocristopathy. Interv Neuroradiol: 2017;1591019917726093 PubMed 28814167
Shun Lu, Shuya Liu, Astrid Wietelmann, Baktybek Kojonazarov, Ann Atzberger, Cong Tang, Ralph Theo Schermuly, Hermann-Josef Gröne, Stefan Offermanns Developmental vascular remodeling defects and postnatal kidney failure in mice lacking Gpr116 (Adgrf5) and Eltd1 (Adgrl4). PLoS ONE: 2017, 12(8);e0183166 PubMed 28806758
Cristina Rodríguez, Miguel Lorenzale, Miguel A López-Unzu, Borja Fernández, Francisca Salmerón, Valentín Sans-Coma, Ana C Durán The bulbus arteriosus of the holocephalan heart: gross anatomy, histomorphology, pigmentation, and evolutionary significance. Zoology (Jena): 2017; PubMed 28760682
Kazuki Kodo, Shinsuke Shibata, Sachiko Miyagawa-Tomita, Sang-Ging Ong, Hiroshi Takahashi, Tsutomu Kume, Hideyuki Okano, Rumiko Matsuoka, Hiroyuki Yamagishi Regulation of Sema3c and the Interaction between Cardiac Neural Crest and Second Heart Field during Outflow Tract Development. Sci Rep: 2017, 7(1);6771 PubMed 28754980
Haig Aghajanian, Young Kuk Cho, Nicholas W Rizer, Qiaohong Wang, Li Li, Karl Degenhardt, Rajan Jain Pdgfrα functions in endothelial-derived cells to regulate neural crest cells and development of the great arteries. Dis Model Mech: 2017; PubMed 28714851
- A L Rosa, M E Alvarez, D Lawson, H J Maccioni A polypeptide of 59 kDa is associated with bundles of cytoplasmic filaments in Neurospora crassa. Biochem. J.: 1990, 268(3);649-55 PubMed 2141976
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Cite this page: Hill, M.A. 2017 Embryology Neural Crest - Cardiac. Retrieved August 23, 2017, from https://embryology.med.unsw.edu.au/embryology/index.php/Neural_Crest_-_Cardiac
- © Dr Mark Hill 2017, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G