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.
Full textAllardyce, 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.
Full textNgamjariyawat, 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.
Full textBallard, 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.
Full textOkeke, 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.
Full textJohnston, 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.
Full textNekooie, Marnany Nioosha. "The Intersection of Metabolism and Neural Crest Cell Development." Electronic Thesis or Diss., Paris 12, 2022. http://www.theses.fr/2022PA120066.
Full textMetabolism 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
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.
Full textDickens, 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.
Full textRossi, 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.
Find full textIncludes bibliographical references (leaves 112-120). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
McLennan, Rebecca. "Expression and function of EphA4 and ephrin-As in avian trunk neural crest migration /." free to MU campus, to others for purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3144440.
Full textDarrigrand, Jean-François. "Influence of BMP signaling on neural crest cells during heart outflow tract septation." Electronic Thesis or Diss., Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2019SORUS085.pdf.
Full textThe heart outflow tract (OFT) is originally a solitary tube, which is septated into the aortic and pulmonary artery (Pa) during embryonic development. This morphogenesis is regulated by the cardiac neural crest cells (cNCC), which colonize the OFT and condense towards the endocardium, triggering its rupture and the fromation of the two arteries. Investigations to identify the molecular cues controlling cNCC behaviour in the OFT mesenchyme have established the importance of the Bone Morphogenic Proteins (BMP). However, little is known on the molecular cascades triggered by BMP signaling responsible for the cNCC mediated OFT septation. To get insights into these molecular cascades, we decided to dissect the role of Dullard, a perinuclear phosphatase uncovered as a BMP intracellular signaling inhibitor, during OFT morphogenesis. Our results show that deletion of Dullard in the cNCC increases BMP intracellular signaling, leading to premature and asymmetric septation of the OFT, Pa obstruction and embryonic death. This BMP overactivation in the cNCC triggers the downregulation of mesenchymal markers and the upregulation of a cytokine called Sema3c, which in turn results in premature cNCC compaction at the endocardium. In addition, asymmetric differentiation of the distal subpulmonary myocardium contributes to asymmetrical rupture of the endocardium and Pa obstruction. Finally, our data converge to a model whereby graded BMP activity and Sema3c expression in the cNCC along the OFT axis set the tempo of OFT septation from its distal to its proximal regions. Hence, our findings reveal that fine tuning of BMP signaling levels in cNCC orchestrate OFT septation in time and space
Frith, Thomas J. R. "Delineating the signals in anterior-posterior patterning of hPSC derived neural crest cells." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/19471/.
Full textYang, Xiu. "ALTERED NEURONAL LINEAGES IN THE FACIAL GANGLIA OF Hoxa2 MUTANT MICE." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1207189742.
Full textMills, Alexandra Noelle. "Wolf-Hirschhorn Syndrome related genes are implicated in neural crest cell migration during development." Thesis, Boston College, 2018. http://hdl.handle.net/2345/bc-ir:108021.
Full textWolf Hirschhorn Syndrome (WHS) is a neurodevelopmental disorder characterized by craniofacial malformations, heart and skeletal defects, intellectual disability as well as seizure disorders. While this disorder is thought to arise from a deletion of a region on the short arm of chromosome 4, which includes the four genes WHSC1, WHSC2, LETM1 and TACC3, the mechanism by which loss of these genes results in WHS is not understood. Given that these genes have been linked to cell migration and that affected tissues include those derived from the neural crest, we propose that WHS results from a defect in neural crest cell migration. Here, we show that WHSC1, WHSC2, TACC3 and LETM1 are all expressed along the neural tube and developing neural folds during Xenopus embryonic development. These genes are additionally enriched in the pharyngeal arches, which are migrating neural crest cells. The knockdown of these WHS-related genes leads to variable defects in craniofacial and cartilage morphology. Moreover, the loss of WHS gene expression causes defects in forebrain and midbrain development. This implicates these four genes in the WHS phenotype. Further analysis of both WHSC1 and TACC3 function show that their individual knockdown causes defective neural crest cell migration both in vivo and in vitro. This supports the notion that the WHS phenotype is a result of erroneous neural crest cell motility. Our analysis shows that the WHS related genes; WHSC1, WHSC2, LETM1 and TACC3, play a role in the WHS phenotype of craniofacial malformation, skeletal abnormality, and microcephaly. Further analysis of these genes will determine the combinatorial effects of their knockdown on neural crest cell migration during embryonic development to further elucidate the mechanism through which WHS develops
Thesis (BS) — Boston College, 2018
Submitted to: Boston College. College of Arts and Sciences
Discipline: Departmental Honors
Discipline: Biology
Fu, Ming, and 付明. "Neural crest cell development in the nervous system of normal gut and in Hirschsprung's disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29281970.
Full textMcKenzie, Ian 1977. "The neural crest origins of skin-derived precursors : an accessible source of myelinating Schwann cells." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=100654.
Full textFoster, K. E. "The role of neural crest cells in the development, organisation and migration of the thymus." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19301/.
Full textMillington, Grethel. "Primary Cilia-dependent Gli Processing in Neural Crest Cells is Required for Early Tongue Development." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1479815997983138.
Full textMarathe, Himangi. "SWI/SNF Chromatin Remodeling Enzymes as Regulators of Neural-crest Derived Cell Differentiation." University of Toledo Health Science Campus / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=mco1374233816.
Full textYoshimatsu, Masayoshi. "In vivo regeneration of rat laryngeal cartilage with mesenchymal stem cells derived from human induced pluripotent stem cells via neural crest cells." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/265189.
Full text新制・課程博士
博士(医学)
甲第23417号
医博第4762号
新制||医||1052(附属図書館)
京都大学大学院医学研究科医学専攻
(主査)教授 松田 秀一特定拠点, 教授 妻木 範行, 教授 安達 泰治
学位規則第4条第1項該当
Doctor of Medical Science
Kyoto University
DFAM
Ainsworth, Sophie Jane. "Avian development and disease : the importance of cranial neural crest cells in understanding cartilage repair strategies." Thesis, University of Brighton, 2009. https://research.brighton.ac.uk/en/studentTheses/3ab2e0e6-4897-4350-b5f4-09353049d1e0.
Full textBrindley, Gemma. "The role of cardiac neural crest cells in the development of the outflow tract of the heart." Thesis, University of Newcastle Upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413391.
Full textKomatsu, Koji. "Meltrin β expressed in cardiac neural crest cells is required for ventricular septum formation of the heart." Kyoto University, 2007. http://hdl.handle.net/2433/135667.
Full textLosa, Llabata Marta. "Gene regulation in embryonic development." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/gene-regulation-in-embryonic-development(8a9efb79-1ca9-409e-89b9-9d66213e593f).html.
Full textPhilip, Beatrice. "An Investigation Into the Molecular Mechanisms and Genes Involved in Hypoxic Signalling Pathways in Neural Crest Derived Tumours." Thesis, Griffith University, 2014. http://hdl.handle.net/10072/367341.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
Matthews, Helen Katherine. "A role for Syndecan-4 and PCP signalling in controlling directional migration of neural crest cells in vivo." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/15955/.
Full textNgamjariyawat, Anongnad, Kyril Turpaev, Svitlana Vasylovska, Elena N. Kozlova, and Nils Welsh. "Co-Culture of Neural Crest Stem Cells (NCSC) and Insulin Producing Beta-TC6 Cells Results in Cadherin Junctions and Protection against Cytokine-Induced Beta-Cell Death." Uppsala universitet, Neuroanatomi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-198839.
Full textHjerling-Leffler, Jens. "Sensory neurons: stem cells and development /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-667-0/.
Full textBradshaw, Lucy. "The-role of neural crest cells in the septation of the cardiac outflow and the effects of vitamin supplementation." Thesis, University of Newcastle upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.485859.
Full textRabadán, Lozano M. Ángeles. "Genetic analysis of neural crest migration: Requirement of Dapper2-mediated inhibition of the Wnt canonical activity." Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/83279.
Full textPoon, Hiu-ching. "A study of the regulatory roles of Hedgehog in the enteric nervous system development by the conditional knockout of Patched1 enteric gene in the enteric neural crest cells." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42841604.
Full textZer, Heba al [Verfasser], and Ralf [Akademischer Betreuer] Smeets. "Enrichment and Characterization of Neural Crest - derived Dental Pulp Stem Cells from Human Dental Pulp / Heba Al-Zer. Betreuer: Ralf Smeets." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2015. http://d-nb.info/106893154X/34.
Full textPoon, Hiu-ching, and 潘曉澄. "A study of the regulatory roles of Hedgehog in the enteric nervous system development by the conditional knockout of Patched1 entericgene in the enteric neural crest cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42841604.
Full textAcuña, Mendoza Soledad. "Sources alternatives de cellules souches pour la bio-ingénierie de la dent." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB101.
Full textNeural crest cells are multipotent progenitor cells that, during embryogenic development, migrate and differentiate into diverse lineages such as melanocytes, smooth muscle, peripheral and enteric neurons, glial cells as well as craniofacial mesenchymatic components, including teeth. In the context of the development of an odontogenic model for tissue engineering, we have generated a new cell line of embryonic stem cells (ES) obtained from blastocysts from crossing Wnt1-CRE mice with fluorescent reporter Rosa26 mT/mT mice. In this Cre/Lox system the cells that have acquired a CN identity and thus expressing Wnt1, will become and remain fluorescent due to the activation of Tomato expression. We have generated a simplified protocol in a monolayer cell culture in defined serum-free medium in order to differentiate the cells into CN cells, named ES-CN cells. Second, we investigated the signals necessary for the odontogenic specification of these ES-CN cells. Our study provides evidence that the Wnt1-CRE/Tomato cell line 1) is a competent ES cell line with the expression of pluripotent markers, a stable karyotype and the ability to differentiate in vitro and in vivo into all the three embryonic germ layers, 2) acquires in vitro a CN identity after induction with our protocol, 3) expresses odontogenic markers in hypoxic culture conditions and 4) is able to interact with an oral epithelium in order to form orofacial skeletal tissues via the tissue reassociation in vitro. This novel cell model should facilitate the understanding of the mechanisms implicated in the ectomesenchymatic interaction, at the base for formation of orofacial skeletal tissues, and will provide the possibility to follow the fate of ES-CN cells tissue engineering models of wounded orofacial structures in general
Sharma, Vipul. "Vangl2 as a key regulator of cell behaviour within the developing cardiac outflow tract : elaborating specific roles in second heart field and neural crest cells." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2611.
Full textAtashpazgargari, S. "A CELL REPROGRAMMING-BASED APPROACH TO STUDY 7Q11.23 GENE DOSAGE IMBALANCES IN WILLIAMS BEUREN SYNDROME AND AUTISM SPECTRUM DISORDER." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/264765.
Full textRepele, Andrea. "Differentiation potential and metabolic analysis of satellite cells and amniotic fluid stem cells." Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3422458.
Full textIl nostro gruppo ha recentemente caratterizzato due distinte popolazioni di cellule satelliti, classificate come cloni a bassa proliferazione (LPC) e ad alta proliferazione (HPC), che si differenziano in termini di proliferazione, potenziale rigenerativo e metabolismo mitocondriale. Nel mio lavoro di dottorato, abbiamo valutato e caratterizzato la loro biologia cellulare con particolare attenzione a quelle differenze intrinseche presenti anche prima della loro clonazione. Infatti, ambo le tipologie clonali possono essere distinte mediante il potenziale di membrana mitocondriale (ΔΨm) subito dopo l’isolamento dalla fibra. Questo dato è in accordo con lo stato ossido riduttivo mitocondriale misurato tramite NAD+/NADH e la quantificazione della produzione di CO2. Questi risultati sono responsabili delle differenze metaboliche e possono essere spiegati dalla diversa espressione dell’enzima glicolitico Pfkfb3. Inoltre la concentrazione mitocondriale del Ca2+ e la sensibilità all’apoptosi sono modificate così come la dimensione della rete mitocondriale. In conclusione, siamo stati in grado di determinare quale clone rappresenta la cellula staminale all’interno della popolazione di cellule satelliti. Queste nuove osservazioni sperimentali rivelano caratteristiche fisiologiche della biologia delle popolazioni delle cellule satelliti prima e dopo la clonazione, mettendo in luce un’eterogeneità intrinseca della cellula satellite. Nella seconda parte della mia tesi abbiamo esplorato la possibilità che le cellule satelliti possano, se opportunamente stimolate, trans-differenziarsi in cellule muscolari lisce. Il sistema nervoso enterico normalmente interagisce con le cellule muscolari per controllare l’attività peristaltica e secretoria della parete intestinale. L’incompleta colonizzazione dell’intestino da parte delle cellule della cresta neurale provoca la malattia di Hirschsprung, caratterizzata da aganglionosi del colon distale. Le neurosfere (NLBs), precursori enterici in grado di auto-rinnovarsi, possono generare neuroni e glia; essere isolate dall’intestino di topi, ratti e umani e sono in grado di colonizzare l'intestino dopo il trapianto. Il nostro obiettivo è di capire la relazione tra i precursori di cellule satelliti (MPCs) e NLBs utilizzando un modello in vitro di co-coltura: questo sarà utile in prospettiva di un approccio di ingegneria tissutale per la rigenerazione intestinale e muscolo scheletrico. I nostri dati hanno evidenziato che NLBs, in presenza di MPCs, sono in grado di formare nuovi miotubi. L’uso di terreni di coltura miogenici ha evidenziato un notevole aumento della differenziazione in senso muscolare, promuovendo la formazione di striature ed aumentando l’espressione di desmina. Dall’altra parte, l’utilizzo di terreni di coltura neurogenici ha mostrato un fenotipo simil neurale. Come prospettive future, dobbiamo comprendere ulteriormente la relazione tra MPCs e NLBs e se le sinapsi sono coinvolte in questo processo; si deve verificare se un loro utilizzo su polimeri biocompatibili ne possa influenzare il comportamento, ed infine è necessaria una conferma dei suddetti dati tramite un’analisi di differenziazione in vivo in muscolo scheletrico e liscio. Nella terza ed ultima fase del mio lavoro, ci siamo focalizzati ad esplorare la possibilità che cellule non-muscolari possano, se opportunamente stimolate, differenziare in senso muscolare liscio. Il nostro obiettivo è stato quello di ottenere cellule muscolari lisce (SMCs) partendo da cellule staminali del fluido amniotico umano (hAFSC). hAFSC sono state trasdotte utilizzando un virus codificante per ZsGreen sotto il promotore αSMA. SMhAFSC così ottenute hanno evidenziate un alto livello d’espressione dei geni del muscolo liscio (come αSMA, desmina, calponina e smoothelin). Queste caratteristiche sono state confermate da molteplici analisi: di immunofluorescenza, dimostrando la positività a marcatori specifici per il muscolo liscio; microscopia a trasmissione elettronica (TEM), dove si verificava l’aumento della presenza di filamenti intermedi, di corpi densi e depositi di glicogeno, modello simile rispetto alle SMCs. Analisi in timelapse di SMhAFSC hanno dimostrato che queste possiedono un potenziale contrattile superiore rispetto hAFSC e studi su singola cellula hanno evidenziato la presenza di canali calcio voltaggio-dipendenti attivati da potassio solamente su SMhAFSC. In conclusione, siamo stati in grado di generare di cellule muscolari lisce funzionali da un precursore nonmuscolare ed in secondo luogo il processo di trasduzione può rappresentare un valido strumento per distinguere e selezionare differenti popolazioni. Questa fase può eventualmente superare il ben noto problema dell’espansione di progenitori di cellule muscolari lisce, rendendo queste cellule suscettibili per approcci d’ingegneria tessutale.
Schizas, Nikos. "Neuroprotection in the Injured Spinal Cord : Novel Strategies using Immunomodulation, Stem cell Transplantation and Hyaluronic acid Hydrogel carriers." Doctoral thesis, Uppsala universitet, Ortopedi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-251477.
Full textFerronha, Tiago Guimaràes. "The contribution of LMO4 to neural development: generatin neuronal subtypes in the dorsal spinal cord and controlling EMT in neural crest cells and Neuroblastoma = La contribución de LMO4 al desarrollo neural: la generación de subtipos neuronales de la médula dorsal espinal y el control de la EMT en las células de la cresta neural y de Neuroblastoma." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/127186.
Full textLa formación del sistema nervioso central requiere la generación de una gran diversidad de neuronas, y la identificación de las señales moleculares que regulan este proceso es por lo tanto crucial. En esta tesis, me he centrado primero en estudiar la función de LMO4 durante la neurogénesis en la médula espinal dorsal. Mediante las electroporación in ovo, en embriones de pollo, como una metodología para modular la actividad LMO4 in vivo, se demostró que LMO4 era prescindible para el mantenimiento de los patrones de progenitores, pero que se requiere para la correcta generación de subtipos concretos de interneuronas dorsales (dI1/3/5). Por otra parte, se demostró que la actividad LMO4 es esencial para la promoción de estas identidades mediante la actividad BMP canónica, y proponemos que LMO4 y Smad1 / 5 forman parte de los complejos de proteínas que impulsan el programa genético de especificación de dI1/3/5. En la segunda parte de la tesis, he estudiado el sistema nervioso periférico, así como tumores que surgen de él. El neuroblastoma es un tumor embrionario derivado de células de la cresta neural. Aprovechando un nuevo marcador desarrollo para el linaje de cresta neural y en base a la hipótesis de que los mecanismos moleculares que median la delaminación de la cresta neural también están involucrados en la propagación del neuroblastoma, identificamos varios genes comunes en el desarrollo de la cresta neural y el neuroblastoma. Una búsqueda posterior de los ortólogos humanos del NBGS (genes expresados en neuroblastoma) observamos que LMO4 se expresa en ambos tipos de células analizadas. Experimentos funcionales en estos dos sistemas modelo revelaron que se requiere la actividad LMO4 durante la invasión de células del neuroblastoma y durante la delaminación de la cresta neural. Además, identificamos LMO4 como un cofactor esencial de Snail2, en la represión de la expresión de cadherina, y por tanto en la transición epitelio mesenchyma de la cresta neural y de las células de neuroblastoma. En conjunto, nuestros resultados sugieren que la asociación de altos niveles de LMO4 con neuroblastomas agresivos depende de la regulación de cadherina y, por tanto, de la invasividad tumoral.
Loison-Robert, Ludwig. "Cellule souche gingivale : origine et multipotence." Thesis, Paris Est, 2016. http://www.theses.fr/2016PESC0083/document.
Full textGingiva is a natural regeneration model thanks to its "ad integrum" healing capability. Gingival fibroblasts are the main actors of this property. These cells, the main cellular component of the gingival connective tissue, regulate the inflammatory responses and healing process. This tissue contains, like many others, mesenchymal stem cells; which also partly explain these regenerative abilities. Moreover, as the gingiva is abundant and easily accessible, the use of these stem cells may interest cell therapy or in vitro model tissues responses. In this work, we demonstrated that Stem Cells Derived from Human Gingiva (SCHG) have common properties with neural crest adult stem cells. These cells can be called "stem cells" for their ability to self-renew, adhere to plastic and to differentiate. First, we have shown that the method and the culture products used for isolation of gingival fibroblasts from gingival biopsy had an influence on the obtained cells. Secondly, an analysis of in vitro clonal populations of gingival fibroblasts has shown that gingival fibroblasts are composed of subpopulations that express specific markers of stem cells and neural crests. In addition to their embryological origin, the study of their multipotency was also characterized after expansion and depending on the used additives. Finally, two examples of using these cells and dental pulp stem cells as a model to study the in vitro biocompatibility of biomaterials have been developed, mimicking oral mucosa or dentin reactions (reparative or reactional)
Workman, Michael J. "Generating 3D human intestinal organoids with an enteric nervous system." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1416570664.
Full textGrapensparr, Liza. "Auxiliary Cells for the Vascularization and Function of Endogenous and Transplanted Islets of Langerhans." Doctoral thesis, Uppsala universitet, Integrativ Fysiologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-327314.
Full textLatta, Elizabeth Janet. "Studies of the tissues and molecules that regulate the migration of cranial neural crest cells in the chicken embryo : roles of Midline 1 and retinoic acid." Thesis, Open University, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527449.
Full textOldenburg, Denise [Verfasser], Beate [Gutachter] Brand-Saberi, and Carsten [Gutachter] Theiß. "The role of the cephalic neural crest cells in the development of the limbal stem cell niche of the chicken cornea / Denise Oldenburg ; Gutachter: Beate Brand-Saberi, Carsten Theiß ; Medizinische Fakultät." Bochum : Ruhr-Universität Bochum, 2018. http://d-nb.info/1171521901/34.
Full textGazquez, Elodie. "Études des interactions fonctionnelles entre l'endothéline-3, les intégrines beta1 et les propriétés élastiques du tissu embryonnaire au cours du développement du système nerveux entérique." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066240/document.
Full textThe enteric nervous system (ENS) is derived from enteric neural crest cells (ENCC) that migrate along the length of the intestine through the gut mesenchyme. During this process, ENCC proliferate and differentiate into glial cells and neurons, which aggregate into ganglia. The aim of my thesis is to study how biochemical and mechanical properties of the gut tissue influence ENCC colonization and fate during embryogenesis. The absence of endothelin-3 (EDN3), a small peptide trapped in the embryonic gut mesenchyme, is one of the causes leading to hirschsprung disease, characterized by an aganglionosis of the distal colon. We highlighted for the first time that EDN3 increases ENCC adhesion properties throught 1-integrins focal adhesions and modulates their protrusion dynamics. Moreover, we evidenced a genetic interaction between Edn3 and Itgb1 during ENS development. Also, it is now well established that mechanical properties of the microenvironment influence fundamental mechanisms such as cell migration and cell fate determination. Thus, we analysed whether the mechanical properties of the ENCC’s environment influence their behaviours. Using biophysical approaches, we evidenced a physiological stiffening of the embryonic gut during its development and showed that ENCC migration in 3D is inhibited above a certain rigidity threshold. Finally, we begun to analyse the influence of the elastic properties of the environment onto enteric progenitor cells differenciation, taking advantage of the neurosphere culture system. All together, our results contribute to the understanding of the molecular and cellular mechanisms driving physiological and pathological ENS ontogenesis
Ferré, François. "Isolation et caractérisation des cellules souches gingivales : étude de leur potentiel multipotent." Phd thesis, Université René Descartes - Paris V, 2013. http://tel.archives-ouvertes.fr/tel-01017172.
Full textGazquez, Elodie. "Études des interactions fonctionnelles entre l'endothéline-3, les intégrines beta1 et les propriétés élastiques du tissu embryonnaire au cours du développement du système nerveux entérique." Electronic Thesis or Diss., Paris 6, 2016. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2016PA066240.pdf.
Full textThe enteric nervous system (ENS) is derived from enteric neural crest cells (ENCC) that migrate along the length of the intestine through the gut mesenchyme. During this process, ENCC proliferate and differentiate into glial cells and neurons, which aggregate into ganglia. The aim of my thesis is to study how biochemical and mechanical properties of the gut tissue influence ENCC colonization and fate during embryogenesis. The absence of endothelin-3 (EDN3), a small peptide trapped in the embryonic gut mesenchyme, is one of the causes leading to hirschsprung disease, characterized by an aganglionosis of the distal colon. We highlighted for the first time that EDN3 increases ENCC adhesion properties throught 1-integrins focal adhesions and modulates their protrusion dynamics. Moreover, we evidenced a genetic interaction between Edn3 and Itgb1 during ENS development. Also, it is now well established that mechanical properties of the microenvironment influence fundamental mechanisms such as cell migration and cell fate determination. Thus, we analysed whether the mechanical properties of the ENCC’s environment influence their behaviours. Using biophysical approaches, we evidenced a physiological stiffening of the embryonic gut during its development and showed that ENCC migration in 3D is inhibited above a certain rigidity threshold. Finally, we begun to analyse the influence of the elastic properties of the environment onto enteric progenitor cells differenciation, taking advantage of the neurosphere culture system. All together, our results contribute to the understanding of the molecular and cellular mechanisms driving physiological and pathological ENS ontogenesis
Radu, Anca Gabriela. "Nouvelles régulations métaboliques exercées par la signalisation LKB1 dans les cellules polarisées : conséquences pour l’ontogénie tissulaire." Thesis, Université Grenoble Alpes (ComUE), 2018. http://www.theses.fr/2018GREAV011/document.
Full textThe tumor suppressor LKB1 codes for a serine/threonine kinase. It acts as a key regulator of cell polarity and energy metabolism partly through the activation of the AMP-activated protein kinase (AMPK), a sensor that adapts energy supply to the nutrient demands of cells facing situations of metabolic stress. To achieve metabolic adaptations, AMPK phosphorylates numerous substrates which inhibit anabolic processes while activating catabolic reactions. In particular, AMPK inhibits the mammalian target of rapamycin (mTOR).During my PhD, based on genetically engineered mouse models, I uncovered that Lkb1 signaling is essential for neural crest cells (NCC) formation. NCC are multipotent cells that originate from the neural tube and give rise to various derivatives including bones and cartilage of the face, pigmented cells in the skin and glial and neural cells in peripheral nerves and the enteric nervous system. I demonstrated that Lkb1 is essential for vertebrate head formation and for the differentiation and maintenance of NCC-derivatives in the peripheral nervous system. I also emphasized that LKB1 is acetylated on lysine 48 by the acetyltransferase GCN5 and that this acetylation could regulates cranial NCC ontogeny and head formation. Furthermore, I discovered that Lkb1 controls NCC-derived glial differentiation through metabolic regulations involving amino acid biosynthesis coupled to pyruvate-alanine cycling upstream of mTOR signaling.Phenotypes due to Lkb1 loss in NCC recapitulate clinical features of human disorders called neurocristopathies and therefore suggest that aberrant Lkb1 metabolic signaling underlies the etiology of these pathologies. Abnormal activation of the tumor suppressor p53 has been described in some NCC disorders and p53 inactivation in neurocristopathy mouse models rescues the pathological phenotype. By using a NCC line that can be cultivated as progenitors or differentiated in glial cells in vitro, I demonstrated that Lkb1 expression in NCC-derivatives controls p53 activation by limiting oxidative DNA damage and prevents the formation of lysosomes filled with oxidized proteins and lipids called lipofuscin granules. Interestingly, activation of mTOR and LKB1/AMPK pathways is governed by amino acid sensors and takes place at the lysosome surface. Lysosomes have been proposed as a signaling hub controlling proteolysis and aging. Thus Lkb1 and p53 signaling could converge especially through lysosome homeostasis thereby potentially impacting cellular aging.Strikingly, Sertoli cells, that are epithelial somatic cells, located in seminiferous tubules in testes, and which govern germ cells maturation and whole testis homeostasis, share similar metabolic functions with glial cells. For example, they secrete lactate and alanine to fuel mitochondria of neighboring cells (germ cells or neurons respectively) to control their survival and maturation. During my PhD, we highlighted that Lkb1 is essential for testis homeostasis and spermatogenesis by regulating Sertoli cell polarity and, as observed in glial cells, energy metabolism through pyruvate-alanine cycling. These data suggest that this particular Lkb1 metabolic regulation is conserved in tissues with similar function.Taken together, these studies reveal the underlying molecular mechanisms that coordinately regulate energy metabolism and cell fate. They provide new insights into NCC development and expand our understanding of the role of LKB1 as an energy metabolic regulator. Finally, my PhD projects uncover the existence of a crosstalk between Lkb1 and p53 and underline its importance in NCC disorders
Bahm, Isabel. "PDGF signalling during Neural Crest Cell migration." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10041758/.
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