Talk:Cardiovascular System - Heart Development
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Cite this page: Hill, M.A. (2024, April 18) Embryology Cardiovascular System - Heart Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Cardiovascular_System_-_Heart_Development |
Coronary vessel development: a unique form of vasculogenesis. http://www.ncbi.nlm.nih.gov/pubmed/14525796
2012
Direct Contact with Endoderm-Like Cells Efficiently Induces Cardiac Progenitors from Mouse and Human Pluripotent Stem Cells
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0046413
Tbx2 and Tbx3 induce atrioventricular myocardial development and endocardial cushion formation
Cell Mol Life Sci. 2012 Apr;69(8):1377-89. Epub 2011 Dec 1.
Singh R, Hoogaars WM, Barnett P, Grieskamp T, Rana MS, Buermans H, Farin HF, Petry M, Heallen T, Martin JF, Moorman AF, 't Hoen PA, Kispert A, Christoffels VM. Source Institut für Molekularbiologie, Medizinische Hochschule Hannover, Germany.
Abstract
A key step in heart development is the coordinated development of the atrioventricular canal (AVC), the constriction between the atria and ventricles that electrically and physically separates the chambers, and the development of the atrioventricular valves that ensure unidirectional blood flow. Using knock-out and inducible overexpression mouse models, we provide evidence that the developmentally important T-box factors Tbx2 and Tbx3, in a functionally redundant manner, maintain the AVC myocardium phenotype during the process of chamber differentiation. Expression profiling and ChIP-sequencing analysis of Tbx3 revealed that it directly interacts with and represses chamber myocardial genes, and induces the atrioventricular pacemaker-like phenotype by activating relevant genes. Moreover, mutant mice lacking 3 or 4 functional alleles of Tbx2 and Tbx3 failed to form atrioventricular cushions, precursors of the valves and septa. Tbx2 and Tbx3 trigger development of the cushions through a regulatory feed-forward loop with Bmp2, thus providing a mechanism for the co-localization and coordination of these important processes in heart development.
PMID 22130515
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3314179
http://link.springer.com/article/10.1007/s00018-011-0884-2/fulltext.html
Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
2011
Zebrafish cardiac development requires a conserved secondary heart field
Development. 2011 Jun;138(11):2389-98.
Hami D, Grimes AC, Tsai HJ, Kirby ML. Source Department of Pediatrics, Duke University, Durham, NC 27710, USA.
Abstract
The secondary heart field is a conserved developmental domain in avian and mammalian embryos that contributes myocardium and smooth muscle to the definitive cardiac arterial pole. This field is part of the overall heart field and its myocardial component has been fate mapped from the epiblast to the heart in both mammals and birds. In this study we show that the population that gives rise to the arterial pole of the zebrafish can be traced from the epiblast, is a discrete part of the mesodermal heart field, and contributes myocardium after initial heart tube formation, giving rise to both smooth muscle and myocardium. We also show that Isl1, a transcription factor associated with undifferentiated cells in the secondary heart field in other species, is active in this field. Furthermore, Bmp signaling promotes myocardial differentiation from the arterial pole progenitor population, whereas inhibiting Smad1/5/8 phosphorylation leads to reduced myocardial differentiation with subsequent increased smooth muscle differentiation. Molecular pathways required for secondary heart field development are conserved in teleosts, as we demonstrate that the transcription factor Tbx1 and the Sonic hedgehog pathway are necessary for normal development of the zebrafish arterial pole.
PMID 21558385
1997
Abnormal patterning of the aortic arch arteries does not evoke cardiac malformations
Dev Dyn. 1997 Jan;208(1):34-47.
Kirby ML, Hunt P, Wallis K, Thorogood P. Source Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta 30912-2000, USA.
Abstract
Ablation of the cardiac neural crest results in abnormal development of the aortic arch arteries leading to altered patterning of the great arteries. The cardiac outflow tract is also affected after neural crest ablation because normally a subset of neural crest cells migrates from the pharyngeal region to form the outflow septum. Using neural crest ablation, it has not been possible to separate the occurrence of aortic arch maldevelopment from cardiac outflow tract dysmorphogenesis. In order to determine whether normal aortic arch artery development is a prerequisite for normal outflow tract development, we have used a combination of antisense treatment with backtransplantation of cardiac neural folds to produce abnormal patterning of the aortic arch arteries. Paralogous groups of Hox messages with their anterior expression domains in pharyngeal arches 3, 4 and 6 were targeted. Antisense targeted to paralogous group 3 Hox message caused aortic arch 3 located within the pharyngeal arch to regress in a manner similar to aortic arch 2, while antisense targeted to paralogous group 5 Hox message caused the appearance of an additional pharyngeal arch containing a novel and completely independent aortic arch artery. Antisense treatment targeting paralogous group 4 Hox message led to no detectable cardiovascular phenotype in the first 6 days of development. While regression of arch artery 3 was associated with abnormal branching patterns of the aorta and pulmonary trunk, this did not involve abnormal separation of the aorta and pulmonary trunks, the semilunar valves or the subvalvular region of the outflow tract. Because none of these changes in pharyngeal or aortic arch artery development was accompanied by abnormal development of the cardiac outflow tract, it appears that normal patterning of the aortic arch arteries is not a prerequisite for normal heart development. Using reverse transcription polymerase chain reaction (RT-PCR) we were unable to detect changes in any of the Hox messages except group 4, thus, using this particular experimental strategy, we are unable to demonstrate or refute that expression of hox genes by cardiac neural crest cells controls aortic arch patterning. Development of the cardiac outflow tract was normal in each instance. This suggests that abnormal aortic arch patterning does not necessarily lead to cardiac malformations.
PMID 8989519
