scholarly journals Epigenetic Regulation of Cardiac Neural Crest Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Shun Yan ◽  
Jin Lu ◽  
Kai Jiao
Keyword(s):  
Neural Crest ◽  
Epigenetic Regulation ◽  
Heart Development ◽  
Congenital Heart ◽  
Heart Diseases ◽  
Heart Defects ◽  
Neural Crest Cells ◽  
Abnormal Development ◽  
Cardiac Neural Crest ◽  
Epigenetic Regulators

The cardiac neural crest cells (cNCCs) is a transient, migratory cell population that contribute to the formation of major arteries and the septa and valves of the heart. Abnormal development of cNCCs leads to a spectrum of congenital heart defects that mainly affect the outflow region of the hearts. Signaling molecules and transcription factors are the best studied regulatory events controlling cNCC development. In recent years, however, accumulated evidence supports that epigenetic regulation also plays an important role in cNCC development. Here, we summarize the functions of epigenetic regulators during cNCC development as well as cNCC related cardiovascular defects. These factors include ATP-dependent chromatin remodeling factors, histone modifiers and DNA methylation modulators. In many cases, mutations in the genes encoding these factors are known to cause inborn heart diseases. A better understanding of epigenetic regulators, their activities and their roles during heart development will ultimately contribute to the development of new clinical applications for patients with congenital heart disease.

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.

scholarly journals Mutation of LRP1 in cardiac neural crest cells causes congenital heart defects by perturbing outflow lengthening

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Jiuann-Huey I. Lin ◽  
Timothy N. Feinstein ◽  
Anupma Jha ◽  
Jacob T. McCleary ◽  
Juan Xu ◽  
...  
Keyword(s):  
Neural Crest ◽  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Heart Defects ◽  
Neural Crest Cells ◽  
Cardiac Neural Crest

Exposure of neural crest cells to elevated glucose leads to congenital heart defects, an effect that can be prevented by N-acetylcysteine

2007 ◽  
Vol 79 (3) ◽  
pp. 231-235 ◽  
Author(s):  
Pauline A. M. Roest ◽  
Liesbeth van Iperen ◽  
Shirley Vis ◽  
Lambertus J. Wisse ◽  
Rob E. Poelmann ◽  
...  
Keyword(s):  
Neural Crest ◽  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Heart Defects ◽  
Neural Crest Cells ◽  
Elevated Glucose

scholarly journals Gap Junction–mediated Cell–Cell Communication Modulates Mouse Neural Crest Migration

1998 ◽  
Vol 143 (6) ◽  
pp. 1725-1734 ◽  
Author(s):  
G.Y. Huang ◽  
E.S. Cooper ◽  
K. Waldo ◽  
M.L. Kirby ◽  
N.B. Gilula ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Neural Crest ◽  
Gap Junction ◽  
Heart Defects ◽  
Neural Crest Cells ◽  
Dominant Negative ◽  
Cardiac Neural Crest ◽  
Gap Junction Communication ◽  
Neural Crest Migration

Previous studies showed that conotruncal heart malformations can arise with the increase or decrease in α1 connexin function in neural crest cells. To elucidate the possible basis for the quantitative requirement for α1 connexin gap junctions in cardiac development, a neural crest outgrowth culture system was used to examine migration of neural crest cells derived from CMV43 transgenic embryos overexpressing α1 connexins, and from α1 connexin knockout (KO) mice and FC transgenic mice expressing a dominant-negative α1 connexin fusion protein. These studies showed that the migration rate of cardiac neural crest was increased in the CMV43 embryos, but decreased in the FC transgenic and α1 connexin KO embryos. Migration changes occurred in step with connexin gene or transgene dosage in the homozygous vs. hemizygous α1 connexin KO and CMV43 embryos, respectively. Dye coupling analysis in neural crest cells in the outgrowth cultures and also in the living embryos showed an elevation of gap junction communication in the CMV43 transgenic mice, while a reduction was observed in the FC transgenic and α1 connexin KO mice. Further analysis using oleamide to downregulate gap junction communication in nontransgenic outgrowth cultures showed that this independent method of reducing gap junction communication in cardiac crest cells also resulted in a reduction in the rate of crest migration. To determine the possible relevance of these findings to neural crest migration in vivo, a lacZ transgene was used to visualize the distribution of cardiac neural crest cells in the outflow tract. These studies showed more lacZ-positive cells in the outflow septum in the CMV43 transgenic mice, while a reduction was observed in the α1 connexin KO mice. Surprisingly, this was accompanied by cell proliferation changes, not in the cardiac neural crest cells, but in the myocardium— an elevation in the CMV43 mice vs. a reduction in the α1 connexin KO mice. The latter observation suggests that cardiac neural crest cells may have a role in modulating growth and development of non–neural crest– derived tissues. Overall, these findings suggest that gap junction communication mediated by α1 connexins plays an important role in cardiac neural crest migration. Furthermore, they indicate that cardiac neural crest perturbation is the likely underlying cause for heart defects in mice with the gain or loss of α1 connexin function.

scholarly journals PlexinA2 and semaphorin signaling during cardiac neural crest development

Development ◽  
2001 ◽  
Vol 128 (16) ◽  
pp. 3071-3080 ◽  
Author(s):  
Christopher B. Brown ◽  
Leonard Feiner ◽  
Min-Min Lu ◽  
Jun Li ◽  
Xiaokui Ma ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neural Crest ◽  
Congenital Heart ◽  
Neural Crest Cells ◽  
Model Systems ◽  
Cardiac Neural Crest ◽  
Neural Crest Development ◽  
The Central Nervous System ◽  
Mouse Lines

Classic studies using avian model systems have demonstrated that cardiac neural crest cells are required for proper development of the cardiovascular system. Environmental influences that perturb neural crest development cause congenital heart defects in laboratory animals and in man. However, little progress has been made in determining molecular programs specifically regulating cardiac neural crest migration and function. Only recently have complex transgenic tools become available that confirm the presence of cardiac neural crest cells in the mammalian heart. These studies have relied upon the use of transgenic mouse lines and fate-mapping studies using Cre recombinase and neural crest-specific promoters. In this study, we use these techniques to demonstrate that PlexinA2 is expressed by migrating and postmigratory cardiac neural crest cells in the mouse. Plexins function as co-receptors for semaphorin signaling molecules and mediate axon pathfinding in the central nervous system. We demonstrate that PlexinA2-expressing cardiac neural crest cells are patterned abnormally in several mutant mouse lines with congenital heart disease including those lacking the secreted signaling molecule Semaphorin 3C. These data suggest a parallel between the function of semaphorin signaling in the central nervous system and in the patterning of cardiac neural crest in the periphery.

scholarly journals Connecting teratogen-induced congenital heart defects to neural crest cells and their effect on cardiac function

2014 ◽  
Vol 102 (3) ◽  
pp. 227-250 ◽  
Author(s):  
Ganga H. Karunamuni ◽  
Pei Ma ◽  
Shi Gu ◽  
Andrew M. Rollins ◽  
Michael W. Jenkins ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Neural Crest ◽  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Heart Defects ◽  
Neural Crest Cells

Congenital Heart Diseases and Biotechnology: Connecting by Connexin

2014 ◽  
Vol 995 ◽  
pp. 85-112
Author(s):  
Naznin Sultana ◽  
Nobuhiro Nakamura ◽  
Shigehisa Hirose ◽  
Koichi Kutsuzawa ◽  
Toshihiro Akaike ◽  
...  
Keyword(s):  
Gap Junction ◽  
Heart Development ◽  
Congenital Heart ◽  
Cellular Proliferation ◽  
Cardiac Tissue ◽  
Heart Diseases ◽  
Heart Defects ◽  
Normal Function ◽  
Congenital Heart Diseases ◽  
Developmental Defects

Heart development is a precisely harmonized process of cellular proliferation, migration, differentiation, and integrated morphogenetic interactions, and therefore it is extremely vulnerable to developmental defects that cause congenital heart diseases (CHD). One of the major causes of CHD has been shown to be the mutations in key cardiac channel-forming proteins namely, connexins (Cxs). Cxs are tetra-spanning transmembrane proteins that form gap junction channels and hemichannels on cellular membrane. They allow passage of small molecules or ions between adjacent cells or between cells and the extracellular environment. Studies have revealed that the spatiotemporal expression of Cxs mainly, Cx31.9, Cx40, Cx43, and Cx45 is essentially involved in early developmental events, morphogenetic transformations, maturation, and functional significance of heart. Our lab and others have shown that mutations in gap junction proteins could result in impaired trafficking, misfolding, and improper channel function of these proteins. It has also been shown that differential expressions of cardiac Cxs are associated with pathophysiological conditions of heart. Collectively, these conditions are coupled with abrogated or modified functionality of relevant channels in cardiac tissue, which are associated with many pathological situations, including CHD. Since CHD are a major cause of morbidity, therefore recovery of such kind of heart defects associated with Cxs is extremely important but remains highly challenging. In this review, we will summarize the role of Cxs in development, morphogenesis, maturation, normal function, and pathology of heart, and propose possible bioengineering techniques to recover defects in cardiac tissues related to the modified functions of Cxs.

scholarly journals Backtransplantation of chick cardiac neural crest cells cultured in LIF rescues heart development

1993 ◽  
Vol 198 (4) ◽  
pp. 296-311 ◽  
Author(s):  
Margaret L. Kirby ◽  
Donna H. Kumiski ◽  
Tammy Myers ◽  
Chris Cerjan ◽  
Noboru Mishima
Keyword(s):  
Neural Crest ◽  
Heart Development ◽  
Neural Crest Cells ◽  
Cardiac Neural Crest ◽  
Cells Cultured
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