Relevant bibliographies by topics / Neural crest cells

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Academic literature on the topic 'Neural crest cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 22 June 2024

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Journal articles on the topic "Neural crest cells"

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Hall, Brian K., and J. Andrew Gillis. "Incremental evolution of the neural crest, neural crest cells and neural crest-derived skeletal tissues." Journal of Anatomy 222, no. 1 (March 14, 2012): 19–31. http://dx.doi.org/10.1111/j.1469-7580.2012.01495.x.

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Hall, Brian K. "Evolutionary Origins of the Neural Crest and Neural Crest Cells." Evolutionary Biology 35, no. 4 (October 21, 2008): 248–66. http://dx.doi.org/10.1007/s11692-008-9033-8.

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Bronner-Fraser, Marianne, and Scott E. Fraser. "Cell lineage analysis of the avian neural crest." Development 113, Supplement_2 (April 1, 1991): 17–22. http://dx.doi.org/10.1242/dev.113.supplement_2.17.

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Neural crest cells migrate extensively and give rise to diverse cell types, including cells of the sensory and autonomic nervous systems. A major unanswered question concerning the neural crest is when and how the neural crest cells become determined to adopt a particular fate. We have explored the developmental potential of trunk neural crest cells in avian embryos by microinjecting a vital dye, lysinated rhodamine dextran (LRD), into individual cells within the dorsal neural tube. We find that premigratory and emigrating neural crest cells give rise to descendants with distinct phenotypes in multiple neural crest derivatives. These results are consistent with the idea that neural crest cells are multipotent prior to their emigration from the neural tube and become restricted in phenotype after emigration from the neural tube either during their migration or at their sites of localization. To determine whether neural crest cells become restricted during their migration, we have microinjected individual trunk neural crest cells with dye shortly after they leave the neural tube or as they migrate through the somite. We find that a majority of the clones derived from migrating neural crest cells appear to be multipotent; individual migrating neural crest cells gave rise to both sensory and sympathetic neurons, as well as cells with the morphological characteristics of Schwann cells, and other nonneuronal cells. Even those clones contributing to only one neural crest derivative often contained both neurofilament-positive and neurofilament-negative cells. These data demonstrate that migrating trunk neural crest cells, like their premigratory progenitors, can be multipotent. They give rise to cells in multiple neural crest derivatives and contribute to both neuronal and non-neuronal elements within a given derivative. Thus, restriction of neural crest cell fate must occur relatively late in migration or at the final destinations.
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Kulesa, P., M. Bronner-Fraser, and S. Fraser. "In ovo time-lapse analysis after dorsal neural tube ablation shows rerouting of chick hindbrain neural crest." Development 127, no. 13 (July 1, 2000): 2843–52. http://dx.doi.org/10.1242/dev.127.13.2843.

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Previous analyses of single neural crest cell trajectories have suggested important roles for interactions between neural crest cells and the environment, and amongst neural crest cells. To test the relative contribution of intrinsic versus extrinsic information in guiding cells to their appropriate sites, we ablated subpopulations of premigratory chick hindbrain neural crest and followed the remaining neural crest cells over time using a new in ovo imaging technique. Neural crest cell migratory behaviors are dramatically different in ablated compared with unoperated embryos. Deviations from normal migration appear either shortly after cells emerge from the neural tube or en route to the branchial arches, areas where cell-cell interactions typically occur between neural crest cells in normal embryos. Unlike the persistent, directed trajectories in normal embryos, neural crest cells frequently change direction and move somewhat chaotically after ablation. In addition, the migration of neural crest cells in collective chains, commonly observed in normal embryos, was severely disrupted. Hindbrain neural crest cells have the capacity to reroute their migratory pathways and thus compensate for missing neural crest cells after ablation of neighboring populations. Because the alterations in neural crest cell migration are most dramatic in regions that would normally foster cell-cell interactions, the trajectories reported here argue that cell-cell interactions have a key role in the shaping of the neural crest migration.
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Raible, D. W., and J. S. Eisen. "Regulative interactions in zebrafish neural crest." Development 122, no. 2 (February 1, 1996): 501–7. http://dx.doi.org/10.1242/dev.122.2.501.

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Zebrafish trunk neural crest cells that migrate at different times have different fates: early-migrating crest cells produce dorsal root ganglion neurons as well as glia and pigment cells, while late-migrating crest cells produce only non-neuronal derivatives. When presumptive early-migrating crest cells were individually transplanted into hosts such that they migrated late, they retained the ability to generate neurons. In contrast, late-migrating crest cells transplanted under the same conditions never generated neurons. These results suggest that, prior to migration, neural crest cells have intrinsic biases in the types of derivatives they will produce. Transplantation of presumptive early-migrating crest cells does not result in production of dorsal root ganglion neurons under all conditions suggesting that these cells require appropriate environmental factors to express these intrinsic biases. When early-migrating crest cells are ablated, late-migrating crest cells gain the ability to produce neurons, even when they migrate on their normal schedule. Interactions among neural crest cells may thus regulate the types of derivatives neural crest cells produce, by establishing or maintaining intrinsic differences between individual cells.
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Liu, J. P., and T. M. Jessell. "A role for rhoB in the delamination of neural crest cells from the dorsal neural tube." Development 125, no. 24 (December 15, 1998): 5055–67. http://dx.doi.org/10.1242/dev.125.24.5055.

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The differentiation of neural crest cells from progenitors located in the dorsal neural tube appears to involve three sequential steps: the specification of premigratory neural crest cell fate, the delamination of these cells from the neural epithelium and the migration of neural crest cells in the periphery. BMP signaling has been implicated in the specification of neural crest cell fate but the mechanisms that control the emergence of neural crest cells from the neural tube remain poorly understood. To identify molecules that might function at early steps of neural crest differentiation, we performed a PCR-based screen for genes induced by BMPs in chick neural plate cells. We describe the cloning and characterization of one gene obtained from this screen, rhoB, a member of the rho family GTP-binding proteins. rhoB is expressed in the dorsal neural tube and its expression persists transiently in migrating neural crest cells. BMPs induce the neural expression of rhoB but not the more widely expressed rho family member, rhoA. Inhibition of rho activity by C3 exotoxin prevents the delamination of neural crest cells from neural tube explants but has little effect on the initial specification of premigratory neural crest cell fate or on the later migration of neural crest cells. These results suggest that rhoB has a role in the delamination of neural crest cells from the dorsal neural tube.
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Serbedzija, G. N., M. Bronner-Fraser, and S. E. Fraser. "Developmental potential of trunk neural crest cells in the mouse." Development 120, no. 7 (July 1, 1994): 1709–18. http://dx.doi.org/10.1242/dev.120.7.1709.

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The availability of naturally occurring and engineered mutations in mice which affect the neural crest makes the mouse embryo an important experimental system for studying neural crest cell differentiation. Here, we determine the normal developmental potential of neural crest cells by performing in situ cell lineage analysis in the mouse by microinjecting lysinated rhodamine dextran (LRD) into individual dorsal neural tube cells in the trunk. Labeled progeny derived from single cells were found in the neural tube, dorsal root ganglia, sympathoadrenal derivatives, presumptive Schwann cells and/or pigment cells. Most embryos contained labeled cells both in the neural tube and at least one neural crest derivative, and numerous clones contributed to multiple neural crest derivatives. The time of injection influenced the derivatives populated by the labeled cells. Injections at early stages of migration yielded labeled progeny in both dorsal and ventral neural crest derivatives, whereas those performed at later stages had labeled cells only in more dorsal neural crest derivatives, such as dorsal root ganglion and presumptive pigment cells. The results suggest that in the mouse embryo: (1) there is a common precursor for neural crest and neural tube cells; (2) some neural crest cells are multipotent; and (3) the timing of emigration influences the range of possible neural crest derivatives.
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Pakhomova, N. Yu, E. L. Strokova, A. A. Korytkin, V. V. Kozhevnikov, A. F. Gusev, and A. M. Zaydman. "History of the study of the neural crest (review)." Сибирский научный медицинский журнал 43, no. 1 (February 23, 2023): 13–29. http://dx.doi.org/10.18699/ssmj20230102.

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The neural crest has long attracted the attention of evolutionary biologists and, more recently, clinical specialists, as research in recent decades has significantly expanded the boundaries of knowledge about the involvement of neural crest and neural crest cells in the development of human pathology. The neural crest and neural crest cells are a unique evolutionarily based embryonic structure. Its discovery completely changed the view of the process of embryogenesis. Knowledge of neural crest development sheds light on many of the most «established» questions of developmental biology and evolution. Our article will reflect on the historical stages of the discovery and study of the neural crest and the impact of this discovery on entrenched ideas about germ layer specificity and the theory of germ layers – the reasoning of the neural crest as the fourth germ layer. The aim of this review is to describe the history of the discovery and study of neural crest and neural crest cells based on an analysis of the literature. In writing this article, an analysis of the scientific literature was conducted using the search terms «neural crest», «neural crest cells», «neural crest cell morphology», «germinal layers» and «embryonic development» in the computer databases PubMed, Scopus, Web of Science, and eLibrary. The depth of the analytical search corresponds to the period of the discovery of the neural crest and the first mention of the neural crest as an embryonic morphological structure in the scientific literature. The information presented confirms the high interest of research scientists and clinical specialists in the study of neural crest and neural crest cells. The involvement of neural crest cells in the formation of somatic and musculoskeletal pathologies has received particular attention in recent decades. The literature sources are represented by 169 full-text manuscripts and monographs mainly in English. Conclusions. Neural crest and neural crest cells are unique evolutionary structures. Regularities of formation, reasons which condition migration, differentiation, interaction of neural crest cells with other structures during embryogenesis as well as their potential, which is realized in postnatal period, continue to be the subject of research up to now.
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Nakagawa, S., and M. Takeichi. "Neural crest emigration from the neural tube depends on regulated cadherin expression." Development 125, no. 15 (August 1, 1998): 2963–71. http://dx.doi.org/10.1242/dev.125.15.2963.

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During the emergence of neural crest cells from the neural tube, the expression of cadherins dynamically changes. In the chicken embryo, the early neural tube expresses two cadherins, N-cadherin and cadherin-6B (cad6B), in the dorsal-most region where neural crest cells are generated. The expression of these two cadherins is, however, downregulated in the neural crest cells migrating from the neural tube; they instead begin expressing cadherin-7 (cad7). As an attempt to investigate the role of these changes in cadherin expression, we overexpressed various cadherin constructs, including N-cadherin, cad7, and a dominant negative N-cadherin (cN390), in neural crest-generating cells. This was achieved by injecting adenoviral expression vectors encoding these molecules into the lumen of the closing neural tube of chicken embryos at stage 14. In neural tubes injected with the viruses, efficient infection was observed at the neural crest-forming area, resulting in the ectopic cadherin expression also in migrating neural crest cells. Notably, the distribution of neural crest cells with the ectopic cadherins changed depending on which constructs were expressed. Many crest cells failed to escape from the neural tube when N-cadherin or cad7 was overexpressed. Moreover, none of the cells with these ectopic cadherins migrated along the dorsolateral (melanocyte) pathway. When these samples were stained for Mitf, an early melanocyte marker, positive cells were found accumulated within the neural tube, suggesting that the failure of their migration was not due to differentiation defects. In contrast to these phenomena, cells expressing non-functional cadherins exhibited a normal migration pattern. Thus, the overexpression of a neuroepithelial cadherin (N-cadherin) and a crest cadherin (cad7) resulted in the same blocking effect on neural crest segregation from neuroepithelial cells, especially for melanocyte precursors. These findings suggest that the regulation of cadherin expression or its activity at the neural crest-forming area plays a critical role in neural crest emigration from the neural tube.
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Chan, W. Y., and P. P. Tam. "A morphological and experimental study of the mesencephalic neural crest cells in the mouse embryo using wheat germ agglutinin-gold conjugate as the cell marker." Development 102, no. 2 (February 1, 1988): 427–42. http://dx.doi.org/10.1242/dev.102.2.427.

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The distribution of the mesencephalic neural crest cells in the mouse embryo was studied by mapping the colonization pattern of WGA-gold labelled cells following specific labelling of the neuroectoderm and grafting of presumptive neural crest cells to orthotopic and heterotopic sites. The result showed that (1) there were concomitant changes in the morphology of the neural crest epithelium during the formation of neural crest cells, in the 4- to 7-somite-stage embryos, (2) the neural crest cells were initially confined to the lateral subectodermal region of the cranial mesenchyme and there was minimal mixing with the paraxial mesoderm underneath the neural plate, (3) labelled cells from the presumptive crest region colonized the lateral cranio-facial mesenchyme, the developing trigeminal ganglion and the pharyngeal arch, (4) the formation of neural crest cells was facilitated by the focal disruption of the basal lamina and the cell-cell interaction specific to the neural crest site and (5) the trigeminal ganglion was colonized not only by neural crest cells but also by cells from the ectodermal placode.
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Dissertations / Theses on the topic "Neural crest cells"

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De, Mattos Coelho Aguiar Juliana. "Mesenchymal potentials of the trunk neural crest cells." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00982495.

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The neural crest (NC) derives from the dorsal borders of the vertebrate neural tube. During development, the NC cells migrate and contribute to the formation of different tissues and organs. Along the anteroposterior axis, the NC gives rise to neurons and glia of the peripheral nervous system and to melanocytes. Furthermore, the cephalic NC yields mesenchymal tissues, which form all facial cartilages and bones, the large part of skull, facial dermis, fat cells and smooth muscle cells in the head. In the trunk of amniotes Vertebrates, these tissues are derived from the mesoderm, not from the NC. In lower Vertebrates, however, the trunk NC generates some mesenchymal tissues, such as in the dorsal fins of zebrafish. The question therefore is raised whether the ability of the NC to produce mesenchymal cells was totally lost in the trunk of amniote Vertebrates during evolution, or if it can still be achieved under specific conditions. This work is interested in uncovering the mesenchymal potential of the avian trunk NC, with special interest in the differentiation into osteoblasts and adipocytes.Our experimental approach was to examine the skeletogenic and adipogenic differentiation potentials of quail trunk NC cells after in vitro culture. Cell differentiation was evidenced by the analysis of lineage-specific genes and markers using in situ hybridization (ISH), immunocytochemistry and RT-PCR. The established culture conditions allowed observation of both skeletogenesis and adipogenesis. Osteogenesis was initially characterized by expression of Runx2, the first transcription factor specific of the osteoprogenitors, which was detected by ISH from 5 days of culture. Later, we observed osteoblast maturation, with the expression of collagen1 protein, osteopontin mRNA and alkaline phosphatase mRNA, until the bone matrix mineralization stage. The trunk NC cells also underwent chondrogenesis, as demonstrated by Sox9, aggrecan and collagen10 mRNA expression, and Alcian blue staining. The observation of the mineralized areas and chondrogenesis suggested that the trunk NC cells in vitro are able to perform endochondral and membranous ossifications. In same culture conditions, the cells differentiated also into adipocytes, identified from 10 days of culture by Oil Red O staining. The mRNAs of the CEBP, PPAR and FABP4 adipogenic markers were detected by RT-PCR from 3 days of culture. For the characterization of bone and adipocyte progenitors, we evaluated the differentiation potential of individual trunk NC cells. The phenotypic analysis of these clonal cultures showed that 76% of the cells generated Runx2-positive osteoblasts. Moreover, most of the clone-forming trunk NC cells were multipotent progenitors endowed with both neural and osteogenic potentials. Furthermore, in another clonal culture condition, adipocytes were found in 35.3% of the clones, and approximately half of them also contained glial and/or melanogenic cells.These results show that the trunk NC cells in vitro are able to differentiate not only in their classical derivatives found in vivo (melanocytes, neurons and glial cells), but also in mesenchymal phenotypes, including adipocytes and osteoblasts. Importantly, as in cephalic NC cells, mesenchymal phenotypes differentiated from multipotent progenitor cells, suggesting that, during evolution, the NC stem cells intended for both mesenchymal and neural fates, had the expression of their mesenchymal potential inhibited in the trunk. Thus, although at the dormant state and not expressed in vivo, a significant mesenchymal potential is present in the trunk NC cells of amniotes Vertebrates and can be disclosed in vitro
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Allardyce, Joanna Marie. "Analysis of Wt1 expression in neural crest cells." Thesis, University of Liverpool, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569213.

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The neural crest is a transient collection of cell, termed neural crest cells (NCCs), which develop during neurulation at the outer extremities of the neural folds between surface ectoderm and the developing neural tube. NCCs del aminate from the crest and migrate throughout the developing embryo and differentiate into many cell types such as melanocytes, peripheral neurons, osteocytes, muscle cells and enteric neurons and glia. With the use of a lineage tracing system (Wtl-Cre X Rosa26R mouse line) it was previously found that cells derived from Wtl-expressing cells have contributed to the post-natal enteric nervous system (ENS), indicating that Wtl must have been expressed in progenitor cells of the ENS during embryonic development. The goal of this project was therefore to identify when and where Wtl is expressed during this process. Data from immunofluorescence studies revealed that Wtl is transiently expressed in Sox10-expressing NCCs when they first begin their migration from the neural crest, at E8.5 in the mouse. Wt1 is then down-regulated in NCCs before they enter the foregut at E9.5. This data has been supported by in situ hybridisation studies, where Wtl has been found in cells of the neural crest at the same time point (E8.5) but Wtl mRNA was not shown to be present at any embryonic stage later than this. In vitro investigations were carried out in order to characterise Wtl in vagal level NCCs, as it is NCCs from this region (opposite somites 1-7) and the sacral neural crest (caudal to somite 28) which have been established as the origin of the ENS. NCCs were characterised by morphology and marker expression over a time-period of 7 days. The results from immunofluorescence experiments revealed co- expression of Wtl and NCC markers, SoxlO, up to 96 hours in culture. After this time-point it was no longer possible to detect these proteins in cultured explants. The neuronal marker ~III Tubulin was detected from 48 hours and was still found to be expressed at high levels after 96 hours when Wtl and NCC markers had ceased to be expressed, suggesting differentiation ofNCCs. Migration assays whereby the rate of migration was determined in NCCs in culture over a period of 48 hours revealed a mean migration rate of oum/hour. These data are relevant for future siRNA Wtl knock-down experiments in NCCs in vitro to investigate the effect of loss of Wtl function on migration rates, cell morphology, and expression patterns following preliminary experiments carried out on kidney stem cells.
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Ngamjariyawat, Anongnad. "The beneficial Effects of Neural Crest Stem Cells on Pancreatic β–cells." Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-233157.

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Patients with type-1 diabetes lose their β-cells after autoimmune attack. Islet transplantation is a co-option for curing this disease, but survival of transplanted islets is poor. Thus, methods to enhance β-cell viability and function as well as methods to expand β-cell mass are required. The work presented in this thesis aimed to study the roles of neural crest stem cells or their derivatives in supporting β-cell proliferation, function, and survival. In co-culture when mouse boundary cap neural crest stem cells (bNCSCs) and pancreatic islets were in direct contact, differentiating bNCSCs strongly induced β-cell proliferation, and these proliferating β-cells were glucose responsive in terms of insulin secretion. Moreover, co-culture of murine bNCSCs with β-cell lines RIN5AH and β-TC6 showed partial protection of β-cells against cytokine-induced β-cell death. Direct contacts between bNCSCs and β-cells increased β-cell viability, and led to cadherin and β-catenin accumulations at the bNCSC/β-cell junctions. We proposed that cadherin junctions supported signals which promoted β-cell survival. We further revealed that murine neural crest stem cells harvested from hair follicles were unable to induce β-cell proliferation, and did not form cadherin junctions when cultured with pancreatic islets. Finally, we discovered that the presence of bNCSCs in co-culture counteracted cytokine-mediated insulin-producing human EndoC-βH1 cell death. Furthermore, these two cell types formed N-cadherin, but not E-cadherin, junctions when they were in direct contact. In conclusion, the results of these studies illustrate how neural crest stem cells influence β-cell proliferation, function, and survival which may improve islet transplantation outcome.
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Ballard, Victoria. "The contribution of extracardiac cells to the developing heart." Thesis, University of Surrey, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250728.

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Okeke, Chukwuebuka. "Role of Nr2f Nuclear Receptors in Controlling Early Neural Crest and Ectomesenchyme Gene Regulation." University of Cincinnati / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1627660719070357.

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Johnston, D. A. "The avian neural crest : behaviour and long-term survival in culture." Thesis, University of Southampton, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376464.

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Nekooie, Marnany Nioosha. "The Intersection of Metabolism and Neural Crest Cell Development." Electronic Thesis or Diss., Paris 12, 2022. http://www.theses.fr/2022PA120066.

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Le métabolisme en tant que clé de voûte du destin des cellules souches fournit non seulement des demandes d'énergie et de molécules précurseurs, mais joue également un rôle dans le remodelage de la chromatine. Dans les embryons de vertébrés, les cellules de la crête neurale (NC) constituent une population remarquable de progéniteurs embryonnaires qui, lors de la délamination du tube neural dorsal, d'une migration et d'une différenciation étendues, donnent lieu à des dérivés neuraux/neuronaux et mésenchymateux. Le potentiel de différenciation des cellules NC nécessite un remodelage épigénétique et des signaux environnementaux. En conséquence, l'intersection du métabolisme et de la lasticité NC fournira des informations essentielles sur la régulation de l'identité et du développement des cellules NC. Ainsi, j'avais l'intention de comprendre le rôle du métabolisme dans l'aspect développemental d'une sous-population de cellules NC, le tronc NC. La première partie de mon étude a abouti à une vision générale des impacts métaboliques sur toutes les étapes de développement de la CN. J'ai mis en évidence que l'oxydation du glucose est un profil métabolique essentiel régissant la délamination, l'adhésion, la migration, la prolifération, le maintien de la tige et la différenciation généralisée des NC. Compte tenu de l'incidence de la transition G1 / S sur l'EMT dans les cellules NC du tronc, l'inhibition de la voie des pentoses phosphates (PPP) n'a pas pu influencer la délamination NC, suggérant une adaptation métabolique pour maintenir les étapes de développement et la survie. Par conséquent, dans l'étape suivante, j'ai cherché à apprécier comment les voies métaboliques s'intègrent dans la délamination NC. Le recâblage de la voie dela glycolyse sous inhibition du PPP au stade de délaminage a fourni un support pour les voies métaboliques multiples recrutées par les progéniteurs NC en réponse au stress métabolique. Mon étude a également élucidé la reprogrammation métabolique du PPP à l'oxydation du glucose dans les cellules NC du tronc, alignée sur la délamination NC à la transition migratoire. De plus, outre le glucose, la glutamine joue un rôle de premier plan dans l'acquisition pluripotente et la délamination des progéniteurs NC qui déclenchent la localisation nucléaire de la glutaminase (GLS) lors de l'étape de délaminage. Par conséquent, la localisation nucléaire du GLS lors de la délamination des cellules NC pré-igratoiressuggère la fonction de régulation du gène pour le GLS. Dans l'ensemble, mes résultats ont indiqué l'intersection du métabolisme et de la reprogrammation NC de l'étape pluripotente à l'engagement NC, définis respectivement par le PPP promu et la localisation nucléaire de GLS au phénotype OXPHOS à base de glucose avec localisation GLS cytoplasmique. De plus, l'interaction possible entre le GLS et la B-caténine a favorisé le nouveau concept sur la contribution du GLS à la signalisation Wnt, prometteuse pour comprendre l'étiologie de nombreuses neurocristopathies
Metabolism as a keystone of stem cells' fate not only supplies demands for energy and precursor molecules but also has roles in chromatin remodeling. In vertebrate embryos, neural crest (NC) cells constitute a remarkable population of embryonic progenitors, which upon delamination from dorsal neural tube, extensive migration and differentiation give rise to both neural/neuronal and mesenchymal derivatives. The developmental potential of NC cells necessitates epigenetic remodeling and environmental cues. Accordingly, the intersection of metabolism and NC plasticity will provide critical insights into the regulation of NC cell identity and development. Thus, I intended to figure out the metabolism role in the developmental aspect of one sub-population of NC cells, trunk type. The first part of my study resulted in a general view of the metabolic impacts on all developmental NC steps. I evidenced that glucose oxidation is a pivotalmetabolic profile governing NC delamination, adhesion, migration, proliferation, maintenance of stemness, and widespread differentiation. Given the incidence of G1/S transition upon EMT in trunk NC cells, the inhibition of pentose phosphate pathway (PPP) was unable to influence the NC delamination, suggesting a metabolic adaptation to maintain developmental steps and survival. Hence, In the next step, I sought to appreciate how metabolic pathways integrate into the NC delamination. The rewiring of glycolysis pathway under PPP suppression in delaminating stage provided support for multi metabolic pathways recruited by NC progenitors in response to the metabolic stress. My study also elucidated the metabolic reprograming from PPP to glucose oxidation in trunk NC cells, aligned with delaminating to migratory transition of these cells. Additionally, besides glucose, glutamine had a prominent role in pluripotent acquisition anddelamination of NC progenitors that triggers the nuclear localization of glutaminase (GLS) upon EMT step. Therefore, the nuclear GLS localization of pre-migratory NC cells in delaminating stage suggests the gene regulatory function for GLS. Altogether, my results indicated the intersection of metabolism and NC reprograming from pluripotent step to the NC commitment, defined respectively by promoted PPP and nuclear localization of GLS to glucose-based OXPHOSphenotype with cytoplasmic GLS localization. Moreover, the possible interaction between GLS and B-catenin fostered the new concept about the contribution of GLS to Wnt signaling, holding promise for understanding the etiology of many neurocristopathies
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Schock, Elizabeth N. B. S. "The Role of Primary Cilia in Neural Crest Cell Development." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1504800027927076.

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Dickens, Claire Julia. "A study of ion regulatory mechanisms in neural crest cells and fibroblasts." Thesis, University of Newcastle Upon Tyne, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287255.

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Rossi, Christy Cortez. "Early development of two cell populations at the neural plate border : rohon-beard sensory neurons and neural crest cells /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.

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Thesis (Ph.D. in Neuroscience) -- University of Colorado Denver, 2008.
Includes bibliographical references (leaves 112-120). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Books on the topic "Neural crest cells"

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Schwarz, Quenten, and Sophie Wiszniak, eds. Neural Crest Cells. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9412-0.

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Hall, Brian K., ed. The Neural Crest and Neural Crest Cells in Vertebrate Development and Evolution. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-09846-3.

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Maya, Sieber-Blum, ed. Neurotrophins and the neural crest. Boca Raton, Fla: CRC Press, 1999.

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Neural Crest Cells. Elsevier, 2014. http://dx.doi.org/10.1016/c2012-0-00698-9.

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Medeiros, Daniel Meulemans, Brian Frank Eames, and Igor Adameyko. Evolving Neural Crest Cells. Taylor & Francis Group, 2020.

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Sieber-Blum, Maya. Neural Crest Stem Cells. WORLD SCIENTIFIC, 2011. http://dx.doi.org/10.1142/8127.

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Medeiros, Daniel Meulemans, Brian Frank Eames, and Igor Adameyko. Evolving Neural Crest Cells. Taylor & Francis Group, 2020.

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Medeiros, Daniel Meulemans, Brian Frank Eames, and Igor Adameyko. Evolving Neural Crest Cells. Taylor & Francis Group, 2020.

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Medeiros, Daniel Meulemans, Brian Frank Eames, and Igor Adameyko. Evolving Neural Crest Cells. Taylor & Francis Group, 2022.

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Medeiros, Daniel Meulemans, Brian Frank Eames, and Igor Adameyko. Evolving Neural Crest Cells. Taylor & Francis Group, 2020.

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Book chapters on the topic "Neural crest cells"

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Troicki, Filip T., Filip T. Troicki, Filip T. Troicki, Carlos A. Perez, Wade L. Thorstad, Brandon J. Fisher, Larry C. Daugherty, et al. "Neural Crest Cells." In Encyclopedia of Radiation Oncology, 537. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_547.

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Dupin, Elisabeth, Giordano W. Calloni, and Nicole M. Le Douarin. "Cell Diversification During Neural Crest Ontogeny: The Neural Crest Stem Cells." In Perspectives of Stem Cells, 47–58. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3375-8_4.

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Hall, Brian K. "Pigment Cells (Chromatophores)." In The Neural Crest and Neural Crest Cells in Vertebrate Development and Evolution, 159–77. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-09846-3_5.

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Simões-Costa, Marcos S., Houman D. Hemmati, Tanya A. Moreno, and Marianne Bronner-Fraser. "Neural Crest Formation and Diversification." In Neural Development and Stem Cells, 123–47. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3801-4_5.

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Chow, Kim Hei-Man, Paul Kwong-Hang Tam, and Elly Sau-Wai Ngan. "Neural Crest and Hirschsprung’s Disease." In Stem Cells and Human Diseases, 353–86. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2801-1_16.

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Hall, Brian K. "Neuronal Cells and Nervous Systems." In The Neural Crest and Neural Crest Cells in Vertebrate Development and Evolution, 179–201. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-09846-3_6.

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Hall, Brian K. "Cartilage Cells and Skeletal Systems." In The Neural Crest and Neural Crest Cells in Vertebrate Development and Evolution, 203–46. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-09846-3_7.

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Dundr, Pavel, and Jiří Ehrmann. "Neural Crest Cell-Derived Tumors: An Overview." In Stem Cells and Cancer Stem Cells, Volume 1, 29–40. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1709-1_4.

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Hall, Brian K. "Embryological Origins and the Identification of Neural Crest Cells." In The Neural Crest and Neural Crest Cells in Vertebrate Development and Evolution, 23–61. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-09846-3_2.

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Moreira, Sofia, Jaime A. Espina, Joana E. Saraiva, and Elias H. Barriga. "A Toolbox to Study Tissue Mechanics In Vivo and Ex Vivo." In Methods in Molecular Biology, 495–515. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2035-9_29.

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AbstractDuring vertebrate embryogenesis, tissues interact and influence each other’s development to shape an embryo. While communication by molecular components has been extensively explored, the role of mechanical interaction between tissues during embryogenesis is just starting to be revealed. Addressing mechanical involvement in morphogenesis has traditionally been challenging mainly due to the lack of proper tools to measure and modify mechanical environments of cells in vivo. We have recently used atomic force microscopy (AFM) to show that the migration of the Xenopus laevis cephalic neural crest cells is triggered by stiffening of the mesoderm, a tissue that neural crest cells use as a migratory substrate in vivo. Interestingly we showed that the activity of the planar cell polarity (PCP) pathway is required to mediate this novel mechanical interaction between two tissues. In this chapter, we share the toolbox that we developed to study the role of PCP signaling in mesoderm cell accumulation and stiffening (in vivo) as well as the impact of mesoderm stiffness in promoting neural crest cell polarity and migration (ex vivo). We believe that these tools can be of general use for investigators interested in addressing the role of mechanical inputs in vivo and ex vivo.
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Conference papers on the topic "Neural crest cells"

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KANAKUBO, SACHIKO, and NORIKO OSUMI. "DEVELOPMENTAL CONTRIBUTION OF NEURAL CREST-DERIVED CELLS IN MURINE EYE STRUCTURES." In Proceedings of the Final Symposium of the Tohoku University 21st Century Center of Excellence Program. IMPERIAL COLLEGE PRESS, 2006. http://dx.doi.org/10.1142/9781860948800_0012.

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Olsen, Rachelle R., Otero Joel, Kirby Wallace, Jerold Rehg, and Kevin W. Freeman. "Abstract A04: Modeling pediatric malignancies by transforming primary neural crest cells." In Abstracts: AACR Special Conference: Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; November 9-12, 2015; Fort Lauderdale, Florida. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.pedca15-a04.

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Olsen, Rachelle R., Joel H. Otero, Jesus Garcia-Lopez, Kirby A. Wallace, Zhirong Yin, and Kevin W. Freeman. "Abstract A19: Transformation of primary neural crest cells to model pediatric cancers." In Abstracts: AACR Special Conference on Developmental Biology and Cancer; November 30 - December 3, 2015; Boston, Massachusetts. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.devbiolca15-a19.

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von Levetzow, Cornelia, Gregor von Levetzow, Jessie H. Hsu, Ron Cole, Romulo Martin Brena, Peter W. Laird, and Elizabeth R. Lawlor. "Abstract LB-233: Modeling Ewing sarcoma initiation in human neural crest stem cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-233.

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Unachukwu, U. J., and J. M. D'Armiento. "Defining the Pathogenic Role of Neural Crest Cells in Lymphangioleiomyomatosis: Mechanistic and Therapeutic Implications." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a6782.

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von Levetzow, Cornelia, Gregor von Levetzow, Jessie H. Hsu, Romulo Martin Brena, Peter W. Laird, and Elizabeth R. Lawlor. "Abstract SY15-01: Modeling the initiation of Ewing sarcoma in human neural crest stem cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-sy15-01.

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Mosher, Jack T., Victor S. Chen, and Elizabeth R. Lawlor. "Abstract 5033: Modeling Ewing's sarcoma and tolerance of EWS-FLI1 with neural crest stem cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5033.

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Chao, P. Grace, Elsa Angelini, Zhongliang Tang, Winston Chang, J. Chloe¨ Bulinski, Alan C. West, and Clark T. Hung. "Novel Application of Microfluidic Channels in Studying Cell Migration and Reorientation in Response to Direct Current Electric Fields." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33138.

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Electric fields have been shown to induce cell migration (galvanotaxis) and cell shape changes (galvanotropism) in many cell types, such as neural crest cells, embryonic cells, and chondrocytes [1–3]. In this study, a novel microfluidic system was developed to study individual cellular responses to applied electric fields. These microfabricated channels are made from commercially available poly-dimethyl-siloxane (PDMS). This gas permeable, tough, and transparent polymer provides a sterile tissue culture environment and permits visualization of cells using epifluorescence microscopy. In conjunction with the device, a custom computer program was written to quantify the migratory behavior of cells by analyzing changes in position and cell shape. The flexibility of the channel geometry allows for a wider range of chamber resistance and applied currents (achieving a particular field strength) that may permit further study into the underlying mechanisms of electric field directed cell migration and orientation.
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Wallace, Kirby, Jesus Garcia-Lopez, Joel Otero, Rachelle Olsen, Chelsea DeVaux, Ashton King, Andrew Davidoff, and Kevin Freeman. "Abstract B30: ARID1A is a haploinsufficient tumor suppressor for N-Myc transformation of neural crest cells." In Abstracts: AACR Special Conference on the Advances in Pediatric Cancer Research; September 17-20, 2019; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-b30.

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Distel, Martin, and David Traver. "Abstract PR01: H-RasG12V overexpression in the central nervous system leads to expansion of oligodendrocyte precursor cells and neural crest cells." In Abstracts: AACR Special Conference: Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; November 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.pedcan-pr01.

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Reports on the topic "Neural crest cells"

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada439284.

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurotibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada411714.

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada422403.

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Addendum. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada458421.

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Bannerman, Peter G. The Functional Role(s) of Neurofibromin During Neural Crest Cell Development. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada398169.

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Bannerman, Peter G. The Functional Role(s) of Neurofibromin During Neural Crest Cell Development. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada411420.

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