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Striking parallels between carotid body glomus cell and adrenal chromaffin cell development.
Hockman D, Adameyko I, Kaucka M, Barraud P, Otani T, Hunt A, Hartwig AC, Sock E, Waithe D, Franck MCM, Ernfors P, Ehinger S, Howard MJ, Brown N, Reese J, Baker CVH
(2018) Dev Biol 444 Suppl 1: S308-S324
MeSH Terms: Adrenal Glands, Animals, Basic Helix-Loop-Helix Transcription Factors, Body Patterning, Carotid Body, Cell Differentiation, Cell Hypoxia, Chick Embryo, Chickens, Chromaffin Cells, Mice, Mice, Knockout, Myelin Proteolipid Protein, Neural Crest, Neurons, Pericytes, Transcription Factors
Show Abstract · Added May 30, 2018
Carotid body glomus cells mediate essential reflex responses to arterial blood hypoxia. They are dopaminergic and secrete growth factors that support dopaminergic neurons, making the carotid body a potential source of patient-specific cells for Parkinson's disease therapy. Like adrenal chromaffin cells, which are also hypoxia-sensitive, glomus cells are neural crest-derived and require the transcription factors Ascl1 and Phox2b; otherwise, their development is little understood at the molecular level. Here, analysis in chicken and mouse reveals further striking molecular parallels, though also some differences, between glomus and adrenal chromaffin cell development. Moreover, histology has long suggested that glomus cell precursors are 'émigrés' from neighbouring ganglia/nerves, while multipotent nerve-associated glial cells are now known to make a significant contribution to the adrenal chromaffin cell population in the mouse. We present conditional genetic lineage-tracing data from mice supporting the hypothesis that progenitors expressing the glial marker proteolipid protein 1, presumably located in adjacent ganglia/nerves, also contribute to glomus cells. Finally, we resolve a paradox for the 'émigré' hypothesis in the chicken - where the nearest ganglion to the carotid body is the nodose, in which the satellite glia are neural crest-derived, but the neurons are almost entirely placode-derived - by fate-mapping putative nodose neuronal 'émigrés' to the neural crest.
Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
0 Communities
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17 MeSH Terms
Pathways to clinical CLARITY: volumetric analysis of irregular, soft, and heterogeneous tissues in development and disease.
Hsueh B, Burns VM, Pauerstein P, Holzem K, Ye L, Engberg K, Wang AC, Gu X, Chakravarthy H, Arda HE, Charville G, Vogel H, Efimov IR, Kim S, Deisseroth K
(2017) Sci Rep 7: 5899
MeSH Terms: Animals, Disease, Female, Humans, Hydrogels, Imaging, Three-Dimensional, Mice, Inbred C57BL, Neural Crest, Neurosecretory Systems, Organogenesis, Pancreas
Show Abstract · Added October 31, 2017
Three-dimensional tissue-structural relationships are not well captured by typical thin-section histology, posing challenges for the study of tissue physiology and pathology. Moreover, while recent progress has been made with intact methods for clearing, labeling, and imaging whole organs such as the mature brain, these approaches are generally unsuitable for soft, irregular, and heterogeneous tissues that account for the vast majority of clinical samples and biopsies. Here we develop a biphasic hydrogel methodology, which along with automated analysis, provides for high-throughput quantitative volumetric interrogation of spatially-irregular and friable tissue structures. We validate and apply this approach in the examination of a variety of developing and diseased tissues, with specific focus on the dynamics of normal and pathological pancreatic innervation and development, including in clinical samples. Quantitative advantages of the intact-tissue approach were demonstrated compared to conventional thin-section histology, pointing to broad applications in both research and clinical settings.
1 Communities
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11 MeSH Terms
miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development.
Kara N, Wei C, Commanday AC, Patton JG
(2017) Dev Biol 429: 321-334
MeSH Terms: Animal Fins, Animals, Branchial Region, Cartilage, Cell Differentiation, Cell Proliferation, Cell Survival, Chondrogenesis, Embryo, Nonmammalian, Focal Adhesion Protein-Tyrosine Kinases, Gene Expression Regulation, Developmental, Gene Knockdown Techniques, MicroRNAs, Morphogenesis, Neural Crest, Zebrafish
Show Abstract · Added August 4, 2017
Cranial neural crest cells are a multipotent cell population that generate all the elements of the pharyngeal cartilage with differentiation into chondrocytes tightly regulated by temporal intracellular and extracellular cues. Here, we demonstrate a novel role for miR-27, a highly enriched microRNA in the pharyngeal arches, as a positive regulator of chondrogenesis. Knock down of miR-27 led to nearly complete loss of pharyngeal cartilage by attenuating proliferation and blocking differentiation of pre-chondrogenic cells. Focal adhesion kinase (FAK) is a key regulator in integrin-mediated extracellular matrix (ECM) adhesion and has been proposed to function as a negative regulator of chondrogenesis. We show that FAK is downregulated in the pharyngeal arches during chondrogenesis and is a direct target of miR-27. Suppressing the accumulation of FAK in miR-27 morphants partially rescued the severe pharyngeal cartilage defects observed upon knock down of miR-27. These data support a crucial role for miR-27 in promoting chondrogenic differentiation in the pharyngeal arches through regulation of FAK.
Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.
0 Communities
1 Members
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16 MeSH Terms
Expression of MYCN in Multipotent Sympathoadrenal Progenitors Induces Proliferation and Neural Differentiation, but Is Not Sufficient for Tumorigenesis.
Mobley BC, Kwon M, Kraemer BR, Hickman FE, Qiao J, Chung DH, Carter BD
(2015) PLoS One 10: e0133897
MeSH Terms: Adrenal Glands, Animals, Apoptosis, Carcinogenesis, Cell Differentiation, Cell Lineage, Cell Proliferation, Ganglia, Sympathetic, Gene Expression Regulation, Male, Mice, Mice, Nude, Multipotent Stem Cells, N-Myc Proto-Oncogene Protein, Neural Crest, Neural Stem Cells, Neuroblastoma, Neurons, Proto-Oncogene Proteins
Show Abstract · Added February 20, 2016
Neuroblastoma is a pediatric malignancy of the sympathetic ganglia and adrenal glands, hypothesized to originate from progenitors of the developing sympathetic nervous system. Amplification of the MYCN oncogene is a genetic marker of risk in this disease. Understanding the impact of oncogene expression on sympathoadrenal progenitor development may improve our knowledge of neuroblastoma initiation and progression. We isolated sympathoadrenal progenitor cells from the postnatal murine adrenal gland by sphere culture and found them to be multipotent, generating differentiated colonies of neurons, Schwann cells, and myofibroblasts. MYCN overexpression in spheres promoted commitment to the neural lineage, evidenced by an increased frequency of neuron-containing colonies. MYCN promoted proliferation of both sympathoadrenal progenitor spheres and differentiated neurons derived from these spheres, but there was also an increase in apoptosis. The proliferation, apoptosis, and neural lineage commitment induced by MYCN are tumor-like characteristics and thereby support the hypothesis that multipotent adrenal medullary progenitor cells are cells of origin for neuroblastoma. We find, however, that MYCN overexpression is not sufficient for these cells to form tumors in nude mice, suggesting that additional transforming mutations are necessary for tumorigenesis.
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19 MeSH Terms
The chick embryo as an expanding experimental model for cancer and cardiovascular research.
Kain KH, Miller JW, Jones-Paris CR, Thomason RT, Lewis JD, Bader DM, Barnett JV, Zijlstra A
(2014) Dev Dyn 243: 216-28
MeSH Terms: Animals, Biomedical Research, Cardiovascular Diseases, Chick Embryo, Heart Valves, Hemodynamics, Models, Animal, Neoplasms, Neovascularization, Physiologic, Neural Crest
Show Abstract · Added March 10, 2014
A long and productive history in biomedical research defines the chick as a model for human biology. Fundamental discoveries, including the description of directional circulation propelled by the heart and the link between oncogenes and the formation of cancer, indicate its utility in cardiac biology and cancer. Despite the more recent arrival of several vertebrate and invertebrate animal models during the last century, the chick embryo remains a commonly used model for vertebrate biology and provides a tractable biological template. With new molecular and genetic tools applied to the avian genome, the chick embryo is accelerating the discovery of normal development and elusive disease processes. Moreover, progress in imaging and chick culture technologies is advancing real-time visualization of dynamic biological events, such as tissue morphogenesis, angiogenesis, and cancer metastasis. A rich background of information, coupled with new technologies and relative ease of maintenance, suggest an expanding utility for the chick embryo in cardiac biology and cancer research.
Copyright © 2013 Wiley Periodicals, Inc.
1 Communities
2 Members
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10 MeSH Terms
An exclusively mesodermal origin of fin mesenchyme demonstrates that zebrafish trunk neural crest does not generate ectomesenchyme.
Lee RT, Knapik EW, Thiery JP, Carney TJ
(2013) Development 140: 2923-32
MeSH Terms: Animal Fins, Animals, Biological Evolution, Embryo, Nonmammalian, Female, Fibroblasts, Male, Mesoderm, Neural Crest, Zebrafish
Show Abstract · Added April 26, 2017
The neural crest is a multipotent stem cell population that arises from the dorsal aspect of the neural tube and generates both non-ectomesenchymal (melanocytes, peripheral neurons and glia) and ectomesenchymal (skeletogenic, odontogenic, cartilaginous and connective tissue) derivatives. In amniotes, only cranial neural crest generates both classes, with trunk neural crest restricted to non-ectomesenchyme. By contrast, it has been suggested that anamniotes might generate derivatives of both classes at all axial levels, with trunk neural crest generating fin osteoblasts, scale mineral-forming cells and connective tissue cells; however, this has not been fully tested. The cause and evolutionary significance of this cranial/trunk dichotomy, and its absence in anamniotes, are debated. Recent experiments have disputed the contribution of fish trunk neural crest to fin osteoblasts and scale mineral-forming cells. This prompted us to test the contribution of anamniote trunk neural crest to fin connective tissue cells. Using genetics-based lineage tracing in zebrafish, we find that these fin mesenchyme cells derive entirely from the mesoderm and that neural crest makes no contribution. Furthermore, contrary to previous suggestions, larval fin mesenchyme cells do not generate the skeletogenic cells of the adult fin, but persist to form fibroblasts associated with adult fin rays. Our data demonstrate that zebrafish trunk neural crest does not generate ectomesenchymal derivatives and challenge long-held ideas about trunk neural crest fate. These findings have important implications for the ontogeny and evolution of the neural crest.
1 Communities
1 Members
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10 MeSH Terms
Isolation and culture of neural crest cells from embryonic murine neural tube.
Pfaltzgraff ER, Mundell NA, Labosky PA
(2012) J Vis Exp : e4134
MeSH Terms: Animals, Cell Separation, Embryo, Mammalian, Humans, Mice, Neural Crest, Neural Tube, Wnt1 Protein
Show Abstract · Added July 10, 2012
The embryonic neural crest (NC) is a multipotent progenitor population that originates at the dorsal aspect of the neural tube, undergoes an epithelial to mesenchymal transition (EMT) and migrates throughout the embryo, giving rise to diverse cell types. NC also has the unique ability to influence the differentiation and maturation of target organs. When explanted in vitro, NC progenitors undergo self-renewal, migrate and differentiate into a variety of tissue types including neurons, glia, smooth muscle cells, cartilage and bone. NC multipotency was first described from explants of the avian neural tube. In vitro isolation of NC cells facilitates the study of NC dynamics including proliferation, migration, and multipotency. Further work in the avian and rat systems demonstrated that explanted NC cells retain their NC potential when transplanted back into the embryo. Because these inherent cellular properties are preserved in explanted NC progenitors, the neural tube explant assay provides an attractive option for studying the NC in vitro. To attain a better understanding of the mammalian NC, many methods have been employed to isolate NC populations. NC-derived progenitors can be cultured from post-migratory locations in both the embryo and adult to study the dynamics of post-migratory NC progenitors, however isolation of NC progenitors as they emigrate from the neural tube provides optimal preservation of NC cell potential and migratory properties. Some protocols employ fluorescence activated cell sorting (FACS) to isolate a NC population enriched for particular progenitors. However, when starting with early stage embryos, cell numbers adequate for analyses are difficult to obtain with FACS, complicating the isolation of early NC populations from individual embryos. Here, we describe an approach that does not rely on FACS and results in an approximately 96% pure NC population based on a Wnt1-Cre activated lineage reporter. The method presented here is adapted from protocols optimized for the culture of rat NC. The advantages of this protocol compared to previous methods are that 1) the cells are not grown on a feeder layer, 2) FACS is not required to obtain a relatively pure NC population, 3) premigratory NC cells are isolated and 4) results are easily quantified. Furthermore, this protocol can be used for isolation of NC from any mutant mouse model, facilitating the study of NC characteristics with different genetic manipulations. The limitation of this approach is that the NC is removed from the context of the embryo, which is known to influence the survival, migration and differentiation of the NC.
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8 MeSH Terms
Enteric nervous system specific deletion of Foxd3 disrupts glial cell differentiation and activates compensatory enteric progenitors.
Mundell NA, Plank JL, LeGrone AW, Frist AY, Zhu L, Shin MK, Southard-Smith EM, Labosky PA
(2012) Dev Biol 363: 373-87
MeSH Terms: Animals, Cell Movement, Enteric Nervous System, Female, Forkhead Transcription Factors, Gene Deletion, Intestines, Mice, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Transgenic, Neural Crest, Neurogenesis, Neuroglia, Repressor Proteins, Stem Cells
Show Abstract · Added December 5, 2013
The enteric nervous system (ENS) arises from the coordinated migration, expansion and differentiation of vagal and sacral neural crest progenitor cells. During development, vagal neural crest cells enter the foregut and migrate in a rostro-to-caudal direction, colonizing the entire gastrointestinal tract and generating the majority of the ENS. Sacral neural crest contributes to a subset of enteric ganglia in the hindgut, colonizing the colon in a caudal-to-rostral wave. During this process, enteric neural crest-derived progenitors (ENPs) self-renew and begin expressing markers of neural and glial lineages as they populate the intestine. Our earlier work demonstrated that the transcription factor Foxd3 is required early in neural crest-derived progenitors for self-renewal, multipotency and establishment of multiple neural crest-derived cells and structures including the ENS. Here, we describe Foxd3 expression within the fetal and postnatal intestine: Foxd3 was strongly expressed in ENPs as they colonize the gastrointestinal tract and was progressively restricted to enteric glial cells. Using a novel Ednrb-iCre transgene to delete Foxd3 after vagal neural crest cells migrate into the midgut, we demonstrated a late temporal requirement for Foxd3 during ENS development. Lineage labeling of Ednrb-iCre expressing cells in Foxd3 mutant embryos revealed a reduction of ENPs throughout the gut and loss of Ednrb-iCre lineage cells in the distal colon. Although mutant mice were viable, defects in patterning and distribution of ENPs were associated with reduced proliferation and severe reduction of glial cells derived from the Ednrb-iCre lineage. Analyses of ENS-lineage and differentiation in mutant embryos suggested activation of a compensatory population of Foxd3-positive ENPs that did not express the Ednrb-iCre transgene. Our findings highlight the crucial roles played by Foxd3 during ENS development including progenitor proliferation, neural patterning, and glial differentiation and may help delineate distinct molecular programs controlling vagal versus sacral neural crest development.
Copyright © 2012 Elsevier Inc. All rights reserved.
3 Communities
3 Members
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16 MeSH Terms
Cranial neural crest ablation of Jagged1 recapitulates the craniofacial phenotype of Alagille syndrome patients.
Humphreys R, Zheng W, Prince LS, Qu X, Brown C, Loomes K, Huppert SS, Baldwin S, Goudy S
(2012) Hum Mol Genet 21: 1374-83
MeSH Terms: Alagille Syndrome, Animals, Blotting, Western, Calcium-Binding Proteins, Cells, Cultured, Craniofacial Abnormalities, Embryo, Mammalian, Female, Fluorescent Antibody Technique, Humans, Immunoenzyme Techniques, Integrases, Intercellular Signaling Peptides and Proteins, Jagged-1 Protein, Membrane Proteins, Mesoderm, Mice, Mice, Inbred C57BL, Mice, Knockout, Morphogenesis, Neural Crest, Phenotype, RNA, Messenger, Real-Time Polymerase Chain Reaction, Receptor, Notch1, Reverse Transcriptase Polymerase Chain Reaction, Serrate-Jagged Proteins, Wnt1 Protein
Show Abstract · Added December 16, 2011
JAGGED1 mutations cause Alagille syndrome, comprising a constellation of clinical findings, including biliary, cardiac and craniofacial anomalies. Jagged1, a ligand in the Notch signaling pathway, has been extensively studied during biliary and cardiac development. However, the role of JAGGED1 during craniofacial development is poorly understood. Patients with Alagille syndrome have midface hypoplasia giving them a characteristic 'inverted V' facial appearance. This study design determines the requirement of Jagged1 in the cranial neural crest (CNC) cells, which encompass the majority of mesenchyme present during craniofacial development. Furthermore, with this approach, we identify the autonomous and non-autonomous requirement of Jagged1 in a cell lineage-specific approach during midface development. Deleting Jagged1 in the CNC using Wnt1-cre; Jag1 Flox/Flox recapitulated the midfacial hypoplasia phenotype of Alagille syndrome. The Wnt1-cre; Jag1 Flox/Flox mice die at postnatal day 30 due to inability to masticate owing to jaw misalignment and poor occlusion. The etiology of midfacial hypoplasia in the Wnt1-cre; Jag1 Flox/Flox mice was a consequence of reduced cellular proliferation in the midface, aberrant vasculogenesis with decreased productive vessel branching and reduced extracellular matrix by hyaluronic acid staining, all of which are associated with midface anomalies and aberrant craniofacial growth. Deletion of Notch1 from the CNC using Wnt1-cre; Notch1 F/F mice did not recapitulate the midface hypoplasia of Alagille syndrome. These data demonstrate the requirement of Jagged1, but not Notch1, within the midfacial CNC population during development. Future studies will investigate the mechanism in which Jagged1 acts in a cell autonomous and cell non-autonomous manner.
1 Communities
2 Members
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28 MeSH Terms
Tfap2a and Foxd3 regulate early steps in the development of the neural crest progenitor population.
Wang WD, Melville DB, Montero-Balaguer M, Hatzopoulos AK, Knapik EW
(2011) Dev Biol 360: 173-85
MeSH Terms: Animals, Base Sequence, Body Patterning, Bone Morphogenetic Proteins, Cell Death, DNA Primers, Embryonic Stem Cells, Forkhead Transcription Factors, Gastrulation, Gene Expression Regulation, Developmental, Genes, p53, Intercellular Signaling Peptides and Proteins, Mutation, Neural Crest, Neurogenesis, Transcription Factor AP-2, Wnt Signaling Pathway, Zebrafish, Zebrafish Proteins
Show Abstract · Added November 13, 2012
The neural crest is a stem cell-like population exclusive to vertebrates that gives rise to many different cell types including chondrocytes, neurons and melanocytes. Arising from the neural plate border at the intersection of Wnt and Bmp signaling pathways, the complexity of neural crest gene regulatory networks has made the earliest steps of induction difficult to elucidate. Here, we report that tfap2a and foxd3 participate in neural crest induction and are necessary and sufficient for this process to proceed. Double mutant tfap2a (mont blanc, mob) and foxd3 (mother superior, mos) mob;mos zebrafish embryos completely lack all neural crest-derived tissues. Moreover, tfap2a and foxd3 are expressed during gastrulation prior to neural crest induction in distinct, complementary, domains; tfap2a is expressed in the ventral non-neural ectoderm and foxd3 in the dorsal mesendoderm and ectoderm. We further show that Bmp signaling is expanded in mob;mos embryos while expression of dkk1, a Wnt signaling inhibitor, is increased and canonical Wnt targets are suppressed. These changes in Bmp and Wnt signaling result in specific perturbations of neural crest induction rather than general defects in neural plate border or dorso-ventral patterning. foxd3 overexpression, on the other hand, enhances the ability of tfap2a to ectopically induce neural crest around the neural plate, overriding the normal neural plate border limit of the early neural crest territory. Although loss of either Tfap2a or Foxd3 alters Bmp and Wnt signaling patterns, only their combined inactivation sufficiently alters these signaling gradients to abort neural crest induction. Collectively, our results indicate that tfap2a and foxd3, in addition to their respective roles in the differentiation of neural crest derivatives, also jointly maintain the balance of Bmp and Wnt signaling in order to delineate the neural crest induction domain.
Copyright © 2011 Elsevier Inc. All rights reserved.
2 Communities
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19 MeSH Terms