scholarly journals Cardiovascular Development and the Colonizing Cardiac Neural Crest Lineage

2007 ◽  
Vol 2 ◽  
pp. 88-111 ◽  
Author(s):  
Paige Snider ◽  
Michael Olaopa ◽  
Anthony B. Firulli ◽  
Simon J. Conway
Keyword(s):  
Neural Crest ◽  
Cardiovascular Development ◽  
Cardiac Neural Crest

scholarly journals Single-cell transcriptomic landscape of cardiac neural crest cell derivatives during embryonic and neonatal development

2019 ◽  
Author(s):  
Xuanyu Liu ◽  
Wen Chen ◽  
Wenke Li ◽  
Ziyi Zeng ◽  
James R. Priest ◽  
...  
Keyword(s):  
Neural Crest ◽  
Single Cell ◽  
Single Molecule ◽  
Neural Crest Cell ◽  
Molecular Signature ◽  
Quiescent State ◽  
Cardiovascular Development ◽  
Neonatal Development ◽  
Cell Lineages ◽  
Cardiac Neural Crest

ABSTRACTRationaleCardiac neural crest cells (CNCCs) contribute greatly to cardiovascular development. A thorough understanding of the cell lineages, transcriptomic states and regulatory networks of CNCC derivatives during normal development is essential for deciphering the pathogenesis of CNCC-associated congenital anomalies. However, the transcriptomic landscape of CNCC derivatives during development has not yet been examined at a single-cell resolution.ObjectiveWe sought to systematically characterize the cell lineages, define the developmental chronology and elucidate the transcriptomic dynamics of CNCC derivatives during embryonic and neonatal development.Methods and ResultsWe performed single-cell transcriptomic sequencing of 34,131 CNCC-derived cells in mouse hearts from eight developmental stages between E10.5 and P7. Through single-cell analyses and single-molecule fluorescence in situ hybridization, we confirmed the presence of CNCC-derived mural cells. Furthermore, we found the transition from CNCC-derived pericytes to microvascular smooth muscle cells, and identified the genes that were significantly regulated during this transition through pseudo-temporal analysis. CNCC-derived neurons first appeared at E10.5, which was earlier than previously recognized. In addition, the CNCC derivatives switched from a proliferative to a quiescent state with the progression of development. Gradual loss of the neural crest molecular signature with development was also observed in the CNCC derivatives. Our data suggested that many CNCC-derivatives had already committed or differentiated to a specific lineage when migrating to the heart. Finally, we characterized some previously unknown subpopulations of CNCC derivatives during development. For example, we found that Penk+ cells, which were mainly localized in outflow tract cushions, were all derived from CNCCs.ConclusionsOur study provides novel insights into the cell lineages, molecular signatures, developmental chronology and state change dynamics of CNCC derivatives during embryonic and neonatal development. Our dataset constitutes a valuable resource that will facilitate future efforts in exploring the role of CNCC derivatives in development and disease.

scholarly journals Cardiovascular Development and the Colonizing Cardiac Neural Crest Lineage

2007 ◽  
Vol 7 ◽  
pp. 1090-1113 ◽  
Author(s):  
Paige Snider ◽  
Michael Olaopa ◽  
Anthony B. Firulli ◽  
Simon J. Conway
Keyword(s):  
Gene Expression ◽  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Cardiovascular Development ◽  
Cardiac Neural Crest ◽  
Neural Crest Cell Migration ◽  
Crest Cell

Although it is well established that transgenic manipulation of mammalian neural crest-related gene expression and microsurgical removal of premigratory chicken andXenopusembryonic cardiac neural crest progenitors results in a wide spectrum of both structural and functional congenital heart defects, the actual functional mechanism of the cardiac neural crest cells within the heart is poorly understood. Neural crest cell migration and appropriate colonization of the pharyngeal arches and outflow tract septum is thought to be highly dependent on genes that regulate cell-autonomous polarized movement (i.e., gap junctions, cadherins, and noncanonicalWnt1pathway regulators). Once the migratory cardiac neural crest subpopulation finally reaches the heart, they have traditionally been thought to participate in septation of the common outflow tract into separate aortic and pulmonary arteries. However, several studies have suggested these colonizing neural crest cells may also play additional unexpected roles during cardiovascular development and may even contribute to a crest-derived stem cell population. Studies in both mice and chick suggest they can also enter the heart from the venous inflow as well as the usual arterial outflow region, and may contribute to the adult semilunar and atrioventricular valves as well as part of the cardiac conduction system. Furthermore, although they are not usually thought to give rise to the cardiomyocyte lineage, neural crest cells in the zebrafish (Danio rerio) can contribute to the myocardium and may have different functions in a species-dependent context. Intriguingly, both ablation of chick andXenopuspremigratory neural crest cells, and a transgenic deletion of mouse neural crest cell migration or disruption of the normal mammalian neural crest gene expression profiles, disrupts ventral myocardial function and/or cardiomyocyte proliferation. Combined, this suggests that either the cardiac neural crest secrete factor/s that regulate myocardial proliferation, can signal to the epicardium to subsequently secrete a growth factor/s, or may even contribute directly to the heart. Although there are species differences between mouse, chick, and Xenopus during cardiac neural crest cell morphogenesis, recent data suggest mouse and chick are more similar to each other than to the zebrafish neural crest cell lineage. Several groups have used the genetically definedPax3(splotch) mutant mice model to address the role of the cardiac neural crest lineage. Here we review the current literature, the neural crest-related role of thePax3transcription factor, and discuss potential function/s of cardiac neural crest-derived cells during cardiovascular developmental remodeling.

scholarly journals The Cardiac Neural Crest Cells in Heart Development and Congenital Heart Defects

2021 ◽  
Vol 8 (8) ◽  
pp. 89
Author(s):  
Shannon Erhardt ◽  
Mingjie Zheng ◽  
Xiaolei Zhao ◽  
Tram P. Le ◽  
Tina O. Findley ◽  
...  
Keyword(s):  
Neural Crest ◽  
Signaling Pathways ◽  
Congenital Heart Defects ◽  
Heart Development ◽  
Congenital Heart ◽  
Heart Defects ◽  
Interventricular Septum ◽  
Neural Crest Cells ◽  
Cardiovascular Development ◽  
Cardiac Neural Crest

The neural crest (NC) is a multipotent and temporarily migratory cell population stemming from the dorsal neural tube during vertebrate embryogenesis. Cardiac neural crest cells (NCCs), a specified subpopulation of the NC, are vital for normal cardiovascular development, as they significantly contribute to the pharyngeal arch arteries, the developing cardiac outflow tract (OFT), cardiac valves, and interventricular septum. Various signaling pathways are shown to orchestrate the proper migration, compaction, and differentiation of cardiac NCCs during cardiovascular development. Any loss or dysregulation of signaling pathways in cardiac NCCs can lead to abnormal cardiovascular development during embryogenesis, resulting in abnormalities categorized as congenital heart defects (CHDs). This review focuses on the contributions of cardiac NCCs to cardiovascular formation, discusses cardiac defects caused by a disruption of various regulatory factors, and summarizes the role of multiple signaling pathways during embryonic development. A better understanding of the cardiac NC and its vast regulatory network will provide a deeper insight into the mechanisms of the associated abnormalities, leading to potential therapeutic advancements.

ROLE OF CARDIAC NEURAL CREST CELLS IN CARDIOVASCULAR DEVELOPMENT

1998 ◽  
Vol 60 (1) ◽  
pp. 267-286 ◽  
Author(s):  
Tony L. Creazzo ◽  
Robert E. Godt ◽  
Linda Leatherbury ◽  
Simon J. Conway ◽  
Margaret L. Kirby
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Cardiovascular Development ◽  
Cardiac Neural Crest

scholarly journals Genetic and Cellular Interaction During Cardiovascular Development Implicated in Congenital Heart Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Kazuki Kodo ◽  
Keiko Uchida ◽  
Hiroyuki Yamagishi
Keyword(s):  
Neural Crest ◽  
Congenital Heart ◽  
Cellular Interaction ◽  
Cardiovascular Development ◽  
Cardiac Neural Crest ◽  
Second Heart Field ◽  
Genomic Architecture ◽  
Heart Field ◽  
First Heart Field ◽  
Mutation Analyses

Congenital heart disease (CHD) is the most common life-threatening congenital anomaly. CHD occurs due to defects in cardiovascular development, and the majority of CHDs are caused by a multifactorial inheritance mechanism, which refers to the interaction between genetic and environmental factors. During embryogenesis, the cardiovascular system is derived from at least four distinct cell lineages: the first heart field, second heart field, cardiac neural crest, and proepicardial organ. Understanding the genes involved in each lineage is essential to uncover the genomic architecture of CHD. Therefore, we provide an overview of recent research progress using animal models and mutation analyses to better understand the molecular mechanisms and pathways linking cardiovascular development and CHD. For example, we highlight our recent work on genes encoding three isoforms of inositol 1,4,5-trisphosphate receptors (IP3R1, 2, and 3) that regulate various vital and developmental processes, which have genetic redundancy during cardiovascular development. Specifically, IP3R1 and 2 have redundant roles in the atrioventricular cushion derived from the first heart field lineage, whereas IP3R1 and 3 exhibit redundancy in the right ventricle and the outflow tract derived from the second heart field lineage, respectively. Moreover, 22q11.2 deletion syndrome (22q11DS) is highly associated with CHD involving the outflow tract, characterized by defects of the cardiac neural crest lineage. However, our studies have shown that TBX1, a major genetic determinant of 22q11DS, was not expressed in the cardiac neural crest but rather in the second heart field, suggesting the importance of the cellular interaction between the cardiac neural crest and the second heart field. Comprehensive genetic analysis using the Japanese genome bank of CHD and mouse models revealed that a molecular regulatory network involving GATA6, FOXC1/2, TBX1, SEMA3C, and FGF8 was essential for reciprocal signaling between the cardiac neural crest and the second heart field during cardiovascular development. Elucidation of the genomic architecture of CHD using induced pluripotent stem cells and next-generation sequencing technology, in addition to genetically modified animal models and human mutation analyses, would facilitate the development of regenerative medicine and/or preventive medicine for CHD in the near future.

scholarly journals Effects of the size of lesions of the cardiac neural crest at various embryonic ages on incidence and type of cardiac defects.

Circulation ◽  
1986 ◽  
Vol 73 (2) ◽  
pp. 360-364 ◽  
Author(s):  
W T Besson ◽  
M L Kirby ◽  
L H Van Mierop ◽  
J R Teabeaut
Keyword(s):  
Neural Crest ◽  
Cardiac Defects ◽  
Cardiac Neural Crest
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