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 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

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

Thymic medullary structures: Microscopical picture of the thymic medullary structures in children with congenital heart defects

Biologia ◽  
2012 ◽  
Vol 67 (1) ◽  
Author(s):  
Renáta Mikušová ◽  
Paulína Gálfiová ◽  
Štefan Polák
Keyword(s):  
Neural Crest ◽  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Heart Defects ◽  
Ventricular Septal Defects ◽  
Electron Microscopic ◽  
Septal Defects ◽  
The Face ◽  
Thymic Medulla ◽  
Thymus Cells

AbstractThe aim of this work is to describe the structure of the thymus, especially its medullary part, in children with congenital heart defects. It is known that development of the thymus and the heart is also influenced by neural crest cells. During the early development of the heart and the thymus cells proliferate and migrate to their primordia. It is known that inadequate cephalic neural crest contribution during development of pharyngeal pouch derivatives results in defective organogenesis of the face, the thymus, parathyroid glands and also the heart. We studied the structure of the thymus in children with congenital heart defects from 0 to 12 years of life at light microscopic and electron-microscopic levels. Thymuses of the patients were surgically removed in the Children’s Cardiocenter in Bratislava. The results of our study confirmed the differences in the medullary structures of thymuses with chosen diagnoses. Hassall’s corpuscles in the thymic medulla were various in size and also in structure and number. The special structures of the thymic medullary region in children with ventricular septal defects and defects of outflow of the heart were big cystic Hassall’s corpuscles. In comparison with a size of Hassall’s corpuscles in normal thymuses the size of Hassall’s corpuscles in studied thymuses suprisingly ranged between 100–250 μm.

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