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

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 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

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 Endocytic Protein Defects in the Neural Crest Cell Lineage and Its Pathway Are Associated with Congenital Heart Defects

2021 ◽  
Vol 22 (16) ◽  
pp. 8816
Author(s):  
Angelo B. Arrigo ◽  
Jiuann-Huey Ivy Lin
Keyword(s):  
Neural Crest ◽  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Cardiac Development ◽  
Heart Defects ◽  
Cell Lineage ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Endocytic Trafficking ◽  
Cardiac Phenotype

Endocytic trafficking is an under-appreciated pathway in cardiac development. Several genes related to endocytic trafficking have been uncovered in a mutagenic ENU screen, in which mutations led to congenital heart defects (CHDs). In this article, we review the relationship between these genes (including LRP1 and LRP2) and cardiac neural crest cells (CNCCs) during cardiac development. Mice with an ENU-induced Lrp1 mutation exhibit a spectrum of CHDs. Conditional deletion using a floxed Lrp1 allele with different Cre drivers showed that targeting neural crest cells with Wnt1-Cre expression replicated the full cardiac phenotypes of the ENU-induced Lrp1 mutation. In addition, LRP1 function in CNCCs is required for normal OFT lengthening and survival/expansion of the cushion mesenchyme, with other cell lineages along the NCC migratory path playing an additional role. Mice with an ENU-induced and targeted Lrp2 mutation demonstrated the cardiac phenotype of common arterial trunk (CAT). Although there is no impact on CNCCs in Lrp2 mutants, the loss of LRP2 results in the depletion of sonic hedgehog (SHH)-dependent cells in the second heart field. SHH is known to be crucial for CNCC survival and proliferation, which suggests LRP2 has a non-autonomous role in CNCCs. In this article, other endocytic trafficking proteins that are associated with CHDs that may play roles in the NCC pathway during development, such as AP1B1, AP2B1, FUZ, MYH10, and HECTD1, are reviewed.

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 Reprogramming Axial Level Identity to Rescue Neural-Crest-Related Congenital Heart Defects

2020 ◽  
Vol 53 (3) ◽  
pp. 300-315.e4 ◽  
Author(s):  
Shashank Gandhi ◽  
Max Ezin ◽  
Marianne E. Bronner
Keyword(s):  
Neural Crest ◽  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Heart Defects

scholarly journals Loss of MicroRNAs in Neural Crest Leads to Cardiovascular Syndromes Resembling Human Congenital Heart Defects

2010 ◽  
Vol 30 (12) ◽  
pp. 2575-2586 ◽  
Author(s):  
Zhan-Peng Huang ◽  
Jian-Fu Chen ◽  
Jenna N. Regan ◽  
Colin T. Maguire ◽  
Ru-Hang Tang ◽  
...  
Keyword(s):  
Neural Crest ◽  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Heart Defects

scholarly journals Ethanol exposure alters early cardiac function in the looping heart: a mechanism for congenital heart defects?

2014 ◽  
Vol 306 (3) ◽  
pp. H414-H421 ◽  
Author(s):  
Ganga Karunamuni ◽  
Shi Gu ◽  
Yong Qiu Doughman ◽  
Lindsy M. Peterson ◽  
Katherine Mai ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Congenital Heart Defects ◽  
Late Stage ◽  
Congenital Heart ◽  
Molecular Mechanisms ◽  
Imaging Modality ◽  
Heart Defects ◽  
Ethanol Exposure ◽  
The Body ◽  
Life Threatening

Alcohol-induced congenital heart defects are frequently among the most life threatening and require surgical correction in newborns. The etiology of these defects, collectively known as fetal alcohol syndrome, has been the focus of much study, particularly involving cellular and molecular mechanisms. Few studies have addressed the influential role of altered cardiac function in early embryogenesis because of a lack of tools with the capability to assay tiny beating hearts. To overcome this gap in our understanding, we used optical coherence tomography (OCT), a nondestructive imaging modality capable of micrometer-scale resolution imaging, to rapidly and accurately map cardiovascular structure and hemodynamics in real time under physiological conditions. In this study, we exposed avian embryos to a single dose of alcohol/ethanol at gastrulation when the embryo is sensitive to the induction of birth defects. Late-stage hearts were analyzed using standard histological analysis with a focus on the atrio-ventricular valves. Early cardiac function was assayed using Doppler OCT, and structural analysis of the cardiac cushions was performed using OCT imaging. Our results indicated that ethanol-exposed embryos developed late-stage valvuloseptal defects. At early stages, they exhibited increased regurgitant flow and developed smaller atrio-ventricular cardiac cushions, compared with controls (uninjected and saline-injected embryos). The embryos also exhibited abnormal flexion/torsion of the body. Our evidence suggests that ethanol-induced alterations in early cardiac function have the potential to contribute to late-stage valve and septal defects, thus demonstrating that functional parameters may serve as early and sensitive gauges of cardiac normalcy and abnormalities.

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