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Dissertations / Theses on the topic 'EphrinA5'

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Published: 4 June 2021
Last updated: 10 February 2022

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1

Gu, Jinmo. "An NF-kappaB - EphrinA5 - Dependent Communication between NG2+ Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1458152802.

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2

Kimura, Kensuke. "Pathway-specific engagement of ephrinA5-EphA4/EphA5 system of the substantia nigra pars reticulata in cocaine-induced responses." Kyoto University, 2011. http://hdl.handle.net/2433/151921.

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3

Teng, Teng. "Molecular guidance of serotonin raphe neurons during development." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066584/document.

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Sérotonine (5-HT) neurones du mésencéphale sont nés de jour embryonnaire 10 à 12, et commencent à étendre axones, peu après la neurogenèse, tant rostrale du télencéphale et caudale du tronc cérébral. Ces projections sont très garantis, mais avec un certain degré d'organisation topographique. Dans le télencéphale, le schéma de la 5-HT innervation provenant de la dorsale (B7, B6) ou de la médiane (B5-B8) se distingue des noyaux. Cependant, il n'y a pas d'études de développement détaillées systématiques chez la souris, qui sont le modèle le plus largement utilisé, en particulier pour les études génétiques. Ces données sont importantes pour rassembler afin d'analyser les effets des mutations de la souris sur la voie moléculaire défini des neurones de la sérotonine. De plus, les molécules de guidage qui dirigent ces neurones du raphé 5-HT à différentes cibles ne sont pas connus. Nous avons effectué de nombreuses études sur l'innervation 5-HT visant à détecter la façon dont la partie dorsale et les noyaux du raphé médian sont ciblées sur des régions différentes du cerveau antérieur au cours du développement.Nous avons étudié le rôle de la signalisation ephrinA-EphA dans le ciblage sélectif. Nos résultats démontrent que l'ARNm EphA5 est exprimé sélectivement dans des sous-populations distinctes de neurones du raphé sérotonine. En particulier, EphA5 présentait le plus haut niveau dans les neurones raphé de la sérotonine dorsale (B7). Les résultats des cultures d'explants in vitro et in vivo électroporation analyses indiquent que les ligands de EphA5 (ephrinA5 et ephrinA3) agissent comme des facteurs répulsifs pour les cônes de croissance de l'axone sérotoninergique. Antérograde traçage dans le ephrinA5 - / - souris ont montré des neurones mauvais ciblage du raphé dorsal projections, y compris la projection sérotoninergique. En particulier, notre analyse de tracer les études montrent que le ciblage des dorsales et raphé médian axones à différentes couches du bulbe olfactif est modifié dans le ephrinA5 KO. Cependant, nous ne savons pas à quel stade de développement de ces altérations se produisent, en particulier si cela reflète un changement dans l'orientation des tracts croissant de fibres, ou si cela reflète la maturation de développement en retard quand axones raphé et garantissent des branches dans les régions cibles spécifiques. Nous avons profité d'une nouvelle méthode morphologique, ce qui permet d'analyser l'étiquetage immunocytochimique dans 3_D. 5-HT immunomarquage, dans la projection du cerveau sérotoninergique dans 3_D. Nos résultats montrent que les fibres sérotoninergiques projetant vers le bulbe olfactif besoin d'un calendrier spécial pour entrer la cible. Le profil d'expression de ephrinA5 suggère que ephrinA5 peut être l'un des facteurs qui modulent ce moment
In mice, serotonin (5-HT) midbrain neurons are born from embryonic day 10 to 12, and start extending axons, shortly after neurogenesis, both rostrally to the telencephalon and caudally to the brainstem. These projections are highly collateralized but with some degree of topographic organization. In the telencephalon, the pattern of 5-HT innervation arising from the dorsal (B7, B6) or the medial (B5-B8) nuclei differs. However, there are no systematic detailed developmental studies in mice, which are the most extensively used model, in particular for genetic studies. Such data are important to gather in order to analyze the effects of mouse mutations on defined molecular pathway of serotonin neurons. Moreover the guidance molecules that direct these 5-HT raphe neurons to different targets are not known. We performed several studies of 5-HT innervation aimed at detecting how the dorsal and median raphe nuclei are targeted to different forebrain regions during development. We investigated the role of ephrinA-EphA signaling in selective targeting. Our results demonstrate that EphA5 mRNA is selectively expressed in distinct subpopulation of serotonin raphe neurons. Particularly, EphA5 exhibited the highest level in dorsal raphe serotonin neurons (B7). The results of in vitro explant cultures and in vivo electroporation analyses indicated that the ligands of EphA5 (ephrinA5 and ephrinA3) act as repellent factors for the serotonergic axon growth cones. Anterograde tracing in the ephrinA5 -/- mice showed mistargeting of dorsal raphe neurons projections, including the serotonergic projection. Particularly, our analysis of tracing studies show that targeting of the dorsal and median raphe axons to different layers of the olfactory bulb is altered in the ephrinA5 KO. However we do not know at what developmental stage these alterations occur, in particular whether this reflects an alteration in the orientation of ascending fiber tracts, or whether this reflects late developmental maturation when raphe axons collateralize and branch in specific target regions. We have taken advantage a new morphological method, which allows analyzing immunocytochemical labeling in 3_D. 5-HT immunolabeling, in whole brain serotonergic projection in 3_D. Our findings show that serotonergic fibers projecting to olfactory bulb require a special timing to enter the target. The expression pattern of ephrinA5 suggests that ephrinA5 can be one of the factors that modulate this timing. Overall, our results show for the first time the implication a guidance molecule for the region-specific and time-specific targeting of serotonin raphe neurons and has implications for the anatomo-functional parsing of raphe cell groups
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4

Gerstmann, Katrin [Verfasser], Jürgen [Akademischer Betreuer] Bolz, Lennart [Akademischer Betreuer] Olsson, and Karl-Friedrich [Akademischer Betreuer] Schmidt. "Der Einfluss von EphrinA5 auf die Proliferation und Identität kortikaler Vorläuferzellen während der embryonalen Neurogenese / Katrin Gerstmann. Gutachter: Jürgen Bolz ; Lennart Olsson ; Karl-Friedrich Schmidt." Jena : Thüringer Universitäts- und Landesbibliothek Jena, 2014. http://d-nb.info/1052020402/34.

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5

Reißenweber, Bettina. "Der Einfluss der Hypoxie auf die Expression und Synthese verschiedener Eph-Rezeptoren und Ephrin-Liganden beim malignen Melanom." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-101756.

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Das maligne Melanom ist die aggressivste Form von Hautkrebs und verschiedene Familien von Rezeptortyrosinkinasen sind an der Entwicklung und der verstärkten Malignität beteiligt. Eph-Rezeptoren stellen die größte Klasse der Rezeptortyrosinkinasen dar und spielen eine wichtige Rolle bei der Tumorangiogenese und -progression. Die Genexpression und Proteinsynthese verschiedener Eph-Rezeptoren und Ephrin-Liganden ist bei vielen Tumorentitäten erhöht. Aus diesem Grund sollten sie sich als Zielproteine für die Entwicklung neuer Radiopharmaka eignen. Zudem zeigen Literaturbefunde einen Einfluss der hypoxischen Zellumgebung auf die Genexpression und die Proteinsynthese verschiedener Eph-Rezeptoren und Ephrin-Liganden. Das Ziel dieser Arbeit war es, Regulationsmechanismen bei verschiedenen Eph-Rezeptoren und Ephrin-Liganden aufzuklären, welche durch ein hypoxisches Umfeld hervorgerufen werden. Dazu wurde neben einem extrinsischen Hypoxiemodell an Monolayerzellkulturen auch ein intrinsisches Hypoxiemodell in Form von Tumorsphäroiden untersucht. Da die Genexpression und die Proteinsynthese von EphA2, EphB4, EphrinA1 und EphrinB2 laut Literatur vom Malignitätsgrad abhängig sind, wurden die metastatischen Melanomzelllinien A375, A2058 und MeWo und die prämetastatische Melanomzelllinie MEL-JUSO verwendet. Die Verifizierung der experimentellen Hypoxie erfolgte durch den etablierten Hypoxiemarker [18F]Fluormisonidazol, sowie dem Nachweis der VEGF-Genexpression unter den verwendeten Kulturbedingungen. Damit konnte die Eignung der hypoxischen Systeme gezeigt werden. Unabhängig vom Hypoxiemodell war in keiner der untersuchten Zelllinien ein Einfluss der Hypoxie auf die Genexpression und Proteinsynthese von EphA2, EphB4, EphrinA1 und EphrinB2 nachweisbar. Ein gesteigerter EphA2-Gehalt in Melanomzellen ist laut Literatur mit einer Erhöhung des Metastasierungspotentials verbunden. Um diesen Einfluss innerhalb einer Zelllinie zu untersuchen, wurden transgene A375-Zellen generiert. Mit dieser Zelllinie fanden Untersuchungen zu verschiedenen Metastasierungseigenschaften statt. Dabei wurde festgestellt, dass sich die Migration der Zellen durch den erhöhten EphA2-Gehalt verringerte, dabei war die hypoxische Umgebung ohne Einfluss. Weiterhin wurde festgestellt, dass der EphA2-Rezeptor das Adhäsionsverhalten von A375-Zellen nicht beeinflusst. Auch ein Einfluss auf das invasive Verhalten konnte nicht festgestellt werden. Eine hypoxische Umgebung war in beiden Fällen nicht von Bedeutung. Aus den Ergebnissen der vorliegenden Arbeit kann geschlussfolgert werden, dass bei den untersuchten Melanomzelllinien keine Regulation der Eph-Rezeptoren und Ephrin-Liganden durch ein hypoxisches Umfeld erfolgt. Durch die ausführliche Charakterisierung des EphA2-Rezeptors in der Arbeit kann jedoch geschlussfolgert werden, dass sich der Rezeptor als potentielles Zielmolekül für die Entwicklung neuer Radiotherapeutika und Radiodiagnostika eignet, nicht jedoch für die Detektion hypoxischer Bereiche in Tumoren. Durch die nunmehr etablierte Generierung von Sphäroiden und einer Zelllinie, welche den Rezeptor verstärkt exprimiert und synthetisiert, stehen nun Zellmodelle für die weiterführende Charakterisierung und Analyse neuer Radiodiagnostika und Radiotherapeutika auf der Basis von Inhibitoren und Antikörper gegen EphA2 zur Verfügung.
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6

Holmberg, Johan. "Ephrins off the beaten path /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-720-7.

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7

Weinges, Stefan. "Molecular dissection of ephrinB reverse signaling." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-57408.

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8

Filosa, Alessandro. "Neuron-glia communication via EphA4-ephrinA3 modulates LTP through glial glutamate transport." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-116043.

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9

Rodenas-Ruano, Alma Ileana. "EphrinB3 and Eph Receptors Regulate Hippocampal Synaptic Function." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/34.

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EphrinB ligands and their Eph receptor tyrosine kinases are known to regulate excitatory synaptic functions in the hippocampus. In the CA3-CA1 synapse, ephrinB ligands are localized to the post-synaptic membrane, while their cognate Eph receptors can be expressed in both pre-and post-synaptic membranes. Previous studies show that interaction of ephrinB molecules with Eph receptors leads to changes in long-term potentiation (LTP), suggesting that reverse signaling through postsynaptic ephrinBs may be required for learning and memory. Our collaborative studies demonstrate that the cytoplasmic domain of ephrinB3, and hence reverse signaling, is not required for ephrinB-dependent learning and memory tasks or for LTP of these synapses. We demonstrate that ephrinB3 null mutants show changes in several synaptic proteins including reduced levels of NMDA receptor subunits. These abnormalities are not observed in ephrinB3lacZ reverse signaling mutants, supporting an Eph receptor forward signaling role for ephrinB3 in these processes. NMDA receptors are important in regulating synaptic functions and plasticity in the adult hippocampus, and Eph receptors have been shown to cluster NMDA receptors to the cell membrane. These studies show that ephrinB3 interacts with EphA4 to regulate plasma membrane levels of NR1 in Cos-1 cells and primary hippocampal neurons. In the absence of ephrinB3, NR1 levels are decreased in synaptosomal membranes, increased in microsomal tissues, but not changed in total extracts. This suggests that ephrinB3 regulates NR1 levels through protein trafficking and not gene transcription. Analysis of protein trafficking confirmed that ephrinB3 specifically interacts with EphA4 receptor to regulate NR1 exocytosis but not endocytosis in both transfected Cos-1 cells and primary hippocampal neurons. We postulate that ephrin-Eph receptor interactions are important mediators of synaptic formation and function, in part, through their regulation of NMDA receptors in the hippocampal synapse. In addition, we find that both ephrinB3KO and ephrinB3lacZ mice show an increased number of excitatory synapses, demonstrating a cytoplasmic-dependent reverse signaling role of ephrinB3 in regulating synapse number. Together, these data suggest that ephrinB3 may act like a receptor to transduce reverse signals to regulate the number of synapses formed in the hippocampus, and that it likely acts to stimulate forward signaling through Eph receptors to modulate NMDA receptor trafficking, LTP and learning.
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10

Foo, Shane Siang Chin. "The role of ephrinB2 in blood vessel development." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446850/.

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The development of the vascular network is a complex process that is controlled by precisely balanced angiogenic and anti-angiogenic factors. Several studies have established that ephrinB2 and its receptor EphB4 are important regulators of angiogenic remodelling in the embryonic vasculature. The ablation of either gene in mice leads to fatal cardiovascular defects and early lethality. As ephrinB2 is expressed in different cell types within blood vessels, specifically in arterial endothelial cells, pericytes and vascular smooth muscle cells, the function of the molecule in each cell population has remained unclear. To determine the role of ephrinB2 expression in the luminal endothelial lining of blood vessels, tissue-specific knockout mice were generated with the Cre-loxP method. The resulting mutants displayed fatal defects in the development of blood vessels and the heart that resembled the phenotype of the global ephrinB2 null mice. This demonstrated that ephrinB2 is essential in the endothelial cells and that its expression in other cell types within the cardiovascular system is not sufficient to compensate for this loss. Pericytes and vascular smooth muscle cells, so-called mural cells, are associated with the endothelium and are essential for the formation of a stable and mature vascular network. To study the role of ephrinB2 in mural cells that express progressively increasing levels of the ligand during the second half of embryonic development, a transgenic mouse line expressing Cre recombinase under the control of a fragment from the PDGFR? gene was established. This permitted the generation of mural cell-specific ephrinB2 knockouts in which the investment of pericytes and smooth muscle cells in the microvasculature was impaired so the vessel wall assembly was defective. Consequently, these mutants displayed oedema, haemorrhaging and presumably died of respiratory arrest. These findings demonstrate that ephrinB2 expression in mural cells is essential for the maturation of the microvessels but apparently not for the remodelling of the endothelium. As insufficient support by mural cells and the resulting increase in blood vessel permeability is a relevant factor in human disease, such as diabetic retinopathy and tumours, the findings presented here argue that the ligand may be a potential target for therapeutic intervention.
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11

Creutzfeldt, Claire. "The role of EphrinA for the retinotopic map formation in mouse visual cortex." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-16896.

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12

Sawamiphak, Suphansa. "EphrinB2 regulates VEGFR2 function in developmental and tumor angiogenesis." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-118766.

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13

Gogaki, Eleni G. "Role of ephrinB2 and EphB4 in mouse retinal angiogenesis." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969679475.

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14

Tosch, Paul. "Investigations of ephrin ligands during development." Title page, abstract and table of contents only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09pht713.pdf.

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"May 2002." Addendum inside back cover. Bibliography: p. 139-157. Aims to isolate ephrin ligands from Drosophila melanogaster and analyse their involvement in Drosophila deveopment. Also investigates the potential of ephrin B-1 as a causative gene in the human condition Aicardi's syndrome.
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15

Essmann, Clara Luise. "The role of ephrinB signaling during synaptic plasticity." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-103918.

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16

Domeisen, Regula Felicitas Sabina. "Der Einfluss der EphB4- und ephrinB2-Expression auf die Tumormetastasierung /." [S.l.] : [s.n.], 2009. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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17

Broggini, Thomas [Verfasser]. "Effects of ephrinB2 – EphB4 signaling on spinal metastasis / Thomas Broggini." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1075757436/34.

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18

Sakanovic, Alenko. "EphrinB2 reverse signaling in endothelial cell migration and actin remodeling." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/27030.

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Angiogenesis, the formation of new blood vessels from preexisting vasculature, is exaggerated in cancer. A ligand that may be involved in angiogenesis is ephrinB2, which upon binding to its cognate receptor on an adjacent cell, becomes phosphorylated on tyrosine residues and transduces an as yet uncharacterized signal inside the cell. To examine reverse signaling pathways mediated by ephrinB2, ephrinB2 mutants were generated in which five tyrosine residues in the cytoplasmic tail were mutated to phenylalanine by site directed mutagenesis to effectively block the putative signal transduction pathways. Upon overexpression of wildtype and mutant ephrinB2 in endothelial cells, cellular phenotype changed drastically, with impeded proliferation and severe impact on actin remodeling. Observed cytoskeletal changes suggested that the Rho-like GTPases were involved in the actin remodeling mediated by the cytoplasmic tail of ephrinB2. Thus, activation of Rac and Rho upon ephrinB2 stimulation with soluble EphB6, a cognate receptor of ephrinB2, was examined. Adenoviral vectors encoding wildype and mutant ephrinB2 were also generated and used to infect endothelial cells. Wounding assays were used to monitor cell migration of ephrinB2 overexpressing cells to characterize the role of ephrinB2 in this process. Our data suggest that ephrinB2 may play an important role in the migration of endothelial cells during angiogenesis and future work will identify the signaling components of this pathway.
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19

Hoffacker, Julius [Verfasser]. "EphB2 und ephrinB1 vermittelte Repulsion in humanen Podozyten / Julius Hoffacker." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2021. http://d-nb.info/1241824177/34.

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20

Langlais, Valentin. "Contrôle de l'activité des récepteurs NMDA par la D-sérine : rôle des récepteurs astrocytaires EphB3 et CB1." Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0211/document.

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Les astrocytes sont des partenaires clés des neurones. Dans l’hippocampe, et tout particulièrement au niveau des synapses CA3-CA1, en libérant la D-sérine, ces cellules gliales régulent l’activité des récepteurs glutamatergiques de type N-methyl-D-aspartate (NMDA) et de ce fait la mémoire synaptique, aussi connue sous le nom de plasticité synaptique à long terme. Cependant, le signal synaptique à l’origine de la libération de la D-sérine par les astrocytes reste à ce jour méconnu. De par des données rapportées dans la littérature nous nous sommes tout particulièrement intéressés aux récepteurs astrocytaires aux ephrins de type B3 (EphB3) et aux endocannabinoïdes de type 1 (CB1). Pour ce faire nous avons principalement utilisé une approche électrophysiologique sur des tranches aiguës d’hippocampe de souris adulte. Dans une première étude, nos données indiquent que l’activation des récepteurs EphB3 augmente la présence de D-sérine synaptique et en conséquence l’activité des récepteurs NMDA synaptiques. A l’inverse, leur inhibition diminue à la fois l’activité des récepteurs NMDA synaptiques et la potentialisation à long-terme qui en dépend (LTP ; une forme de plasticité synaptique à long terme). L’interaction EphB3-ephrinB3 contrôle donc la LTP en contrôlant la disponibilité en D-sérine synaptique. Dans une seconde étude, nous avons utilisé un modèle transgénique permettant d’inhiber l’expression des récepteurs CB1 astrocytaires (souris GFAP-CB1-KO). Nous avons découvert que la suppression de ces récepteurs diminue la disponibilité en D-sérine synaptique. De plus, nos travaux montrent que les récepteurs CB1 astrocytaires sont nécessaires à l’induction de la LTP via la D-serine. En conclusion, ces travaux de Thèse révèlent que les récepteurs astrocytaires EphB3 et CB1 régulent les fonctions dépendantes des récepteurs NMDA via le contrôle qu’ils exercent sur la disponibilité en D-sérine
Astrocytes are key partners of neurons. In the hippocampus, and more particularly at CA3-CA1 synapses, by releasing D-serine, these glial cells regulate the activity of synaptic Nmethyl-D-aspartate (NMDA) receptors and thus synaptic memory, also known as long-term synaptic plasticity. Yet, the synaptic signal inducing D-serine release by astrocytes is still unknown. Based on interesting data from the literature we have investigated the role of the astrocytic receptors for ephrinB3 (EphB3) and endocannabinoids (CB1). To this end we used electrophysiological approaches on acute hippocampal slices of adult mice. In a first study, our data indicate on one hand that the activation of EphB3 receptors increases synaptic D-serine availability and in consequences the activity of synaptic NMDA receptor activity. On the other hand, inhibition of EphB3 receptors induces a decrease of synaptic NMDA receptor activity as well as the induction of the long-term potentiation (LTP; a form of long-term plasticity). Thus, EphB3-ephrinB3 interaction controls LTP induction through the availability of synaptic D-serine. In a second study, we used a transgenic model allowing the inhibition of CB1 receptors expression in astrocytes (GFAP-CB1-KO mice). We discovered that their deletion reduced synaptic D-serine availability. Our work shows that astrocytic CB1 receptors are necessary for LTP induction via this D-serine. All together, this PhD work reveals that astrocytic EphB3 and CB1 receptors regulate synaptic NMDA receptor functions through the control of D-serine availability
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Brodie, James Cameron. "Investigation of ephrin regulation during hindbrain segmentation." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249431.

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22

Eberhart, Johann. "EphA4/Ephrin interactions in motor axon guidance /." free to MU campus, to others for purchase, 2002. http://wwwlib.umi.com/cr/mo/fullcit?p3060095.

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23

Schmidt, Tim Sebastian. "Ephrin-B2 overexpression in the vascular endothelium." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1446088/.

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Previous work has established that Eph family receptor tyrosine kinases and ephrin ligands control a wide range of morphogenetic processes in vertebrate embryos through cell-contact dependent signalling interactions. In the developing cardiovascular system, ephrin-B2, a transmembrane protein is expressed by arterial endothelial cells (ECs) whereas the cognate receptor EphB4 is predominantly found on the venous endothelium. Gene targeting studies in mice have demonstrated that both molecules are critically required for angiogenic remodelling of embryonic blood vessels and survival beyond midgestation. To gain more insight into the role of ephrin-B2 in vascular development and its arterial expression, I have used the tetracycline-controlled expression systems to overexpress the ligand in the endothelium of all vascular beds (i.e. in arteries, veins and microvessels) of transgenic mice. In the course of this study, I have employed several different transgenic EC-specific driver lines in combination with tetracycline-controlled (tTA, Tet-OFF) and reverse tetracycline-controlled (rtTA, Tet-ON) transactivators. Ephrin-B2 overexpression triggers enhanced activation of EphB receptors particularly in the venous endothelium. This leads to severe vascular malformations such as oedema and haemorrhaging. Induction of ephrin-B2 expression at different stages of embryonic development controls not only vascular patterning and the recruitment of supporting pericytes and vascular smooth muscle cells but it can also trigger tissue-specific responses. In summary, my work has established that ephrin-B2 is an important regulator of blood vessel morphogenesis throughout embryonic development. Some results suggest that the ligand may also be involved in pathological conditions such as fibrosis as ectopic expression of ephrin-B2 in the embryonic liver triggers the activation of hepatic stellate cells. The resulting increase in matrix deposition around hepatic blood vessels could represent early signs of a fibrotic phenotype.
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Jungas, Thomas. "Caractérisation du rôle de la signalisation Eph-éphrine dans la division cellulaire." Thesis, Toulouse 3, 2015. http://www.theses.fr/2015TOU30102/document.

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Au sein d'un organisme les cellules se divisent et assurent la croissance, la différentiation et l'homéostasie des tissus. Des travaux récents proposent qu'elles communiquent activement entre voisines au sein des organes solides pour coordonner leur propre division et la préservation de l'intégrité tissulaire. Nous proposons que la signalisation Eph-éphrine, acteur de la communication cellulaire locale, participe à cette coordination entre division cellulaire et cohésion du tissu. Au cours de ma thèse, j'ai démontré dans plusieurs modèles cellulaires que la signalisation Eph-éphrine contrôle la division cellulaire et peut induire des retards dans l'abscission et de la polyploïdie. J'ai prouvé par vidéomicrosocpie que ces défauts d'abscission dépendent du domaine catalytique du récepteur EphB2 et de l'activation de la protéine tyrosine kinase relais c-Src. En cascade, c-Src phosphoryle un régulateur clé de la stabilité du pont intercellulaire, la protéine citron kinase (CitK). J'ai également observé que CitK était anormalement localisé durant la cytocinése en aval de la voie Eph. Par des essais kinase in vitro, j'ai exclu une phosphorylation directe de CitK par le récepteur Eph et identifié c-Src comme capable de phosphoryler directement CitK. J'ai identifié les résidus tyrosines de CitK phosphorylés par c-Src, mutés deux d'entre eux et à l'aide d'analyses de sauvetage phénotypique, démontré que ces résidus étaient nécessaires et suffisants pour induire des défauts d'abscission. J'ai ensuite validé in vivo ce rôle original de la voie Eph-éphrine, dans le contexte du développement neuronal chez la souris. Plusieurs membres de la famille des Eph-éphrines sont exprimés dans les progéniteurs neuraux à l'origine des neurones corticaux et des auteurs ont montrés que CitK contrôle la cytocinèse de ces cellules. En utilisant un système Cre-lox, j'ai spécifiquement éteint la signalisation Eph dans ces progéniteurs et observé une modification de la ploïdie neuronale dans ces animaux. J'ai également observé dans les progéniteurs neuraux une co-localisation physiologique de résidus tyrosines phosphorylés et de la protéine CitK, qui adopte un enrichissement apical caractéristique. Ces résultats suggèrent notamment que la signalisation Eph-éphrine pourrait contrôler l'abscission des progéniteurs neuraux via la phosphorylation de CitK. La cytocinèse est aujourd'hui décrite comme un processus cellulaire autonome orchestré par la machinerie intracellulaire. Les résultats obtenus durant mon doctorat suggèrent que la cytocinèse est également régulée par l'environnement local de la cellule comme j'en ai fait la démonstration avec la signalisation Eph-éphrine. D'autre part, mes travaux suggèrent que la phosphorylation de CitK sert d'interrupteur moléculaire durant la progression à travers la division cellulaire et le contrôle de la ploïdie des neurones
Cells within an organism successfully divide to ensure growth, differentiation and homeostasie. Recent work suggests that dividing cells actively communicate with neighbours thus spatially and temporally coordinating cell division while maintaining tissue cohesiveness. We hypothesized that Eph-ephrin signalling, a local cell-cell signalling pathway, could participate in coordinating cell division within a tissue. Using vertebrate and invertebrate cell culture models I showed that Eph-signalling controls cell division and induces delay in the abscission of nascent daughter cells as well as polyploidy. Using time-lapse imaging I proved that the Eph-mediated abscission failure depends on the catalytic activity of the receptor via the non receptor tyrosine kinase relay molecule c-Src. Downstream of Eph signalling c-Src phosphorylates the protein citron kinase (CitK) a well known regulator of intercellular bridge stability. I also observed that CitK was abnormally localized during cytokinesis when Eph signalling was active. Further, using in vitro kinase assays, I demonstrated that Eph does not directly phosphorylate CitK but that c-Src could do so. In addition, using Mass Spectrometry I mapped all tyrosine residues directly phosphorylated by c-Src. I mutated two of them located in the Rho binding domain of CitK and demonstrated that phosphorylation of those residues are necessary and sufficient to induce cytokinesis failure. I validated in vivo this novel role of Eph-ephrin signalling in a physiological context in the developing mouse neocortex. Members of the Eph/ephrin family are expressed in neural progenitors that give rise to neurons of the cortex upon neurogenic division. Importantly, CitK has been shown by others to control cytokinesis of these progenitor cells. Using the Cre-lox system, I specifically turned off Eph forward signalling in neural progenitor cells and observed an alteration of neuronal ploidy in these mutant animals. Further, I also observed that CitK which adopts a particular apical localisation in neural progenitors physiologically co-localized with phosphorylated tyrosine residues. Altogether, these results suggest that Eph-ephrin signalling controls abscission of neural progenitors by promoting phosphorylation of CitK. The textbook view of cytokinesis is that it is a cell autonomous event orchestrated by the intracellular machinery. Data obtained during my PhD suggest that cytokinesis is also regulated by local environment, here Eph/ephrin signalling, and that phosphorylation of CitK may represent a molecular switch in the normal progression of cell division and in the control of neuronal ploidy
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25

Chen, Inn-Inn. "The role of ephrinB2 in hematopoietic stem/progenitor cell differentiation from an arterial hemogenic endothelium." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:3a561742-155f-447e-beb6-42ede41d9bb5.

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During development, hematopoiesis develops in temporally distinct waves in the yolk sac (YS) and embryo proper, culminating in the emergence of definitive hematopoietic stem cells (HSCs) from the hemogenic endothelium (HE) of the dorsal aorta. The close association of this aortic endothelium with definitive hematopoiesis suggests a functional relationship between arteriogenesis and blood development, but this association is not fully understood. To gain insight into this relationship, we have chosen to study the role of the “arterial” marker, EphrinB2 (EfnB2) in hematopoietic specification. EfnB2 is a transmembrane protein critical for the development of the arterial vascular system. We find that EfnB2 is expressed in the VE-Cadh+CD41- HE in Day 2 BL-CFC (blast-colony forming cell) culture and Day 6 EBs (embryoid bodies), and that EfnB2 expression in ES cell differentiation enriches for endothelial cells with greater hemogenic capacity. Knock-down experiments in ES cells showed that EfnB2 is not required for endothelial cell commitment and survival. It is also not required for early hematopoietic commitment and differentiation from EBs or BL-CFCs. However, we find that EfnB2 is required for the maturation of ES cells into CD41+/CD45+ hematopoietic cells in OP9 co-culture and for definitive hematopoietic colony formation in MethoCult3434 medium. This requirement for EfnB2 expression was confirmed by peptide-mediated blocking of EfnB2 binding to its cognate receptors and by forced expression of a phospho-tyrosine signaling-deficient EfnB2. These results provide evidence for an essential role of endothelial EfnB2 in hematopoiesis.
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26

Prévost, Nicolas. "Les interactions entre plaquettes assurent l'irreversibilité de l'agrégation plaquettaire : un rôle pour les récepteurs Eph et ephrines." Paris 7, 2004. http://www.theses.fr/2004PA077222.

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27

Zimmer, Manuel. "Mechanisms of Eph, ephrin mediated cell-cell communication." Diss., [S.l.] : [s.n.], 2003. http://edoc.ub.uni-muenchen.de/archive/00001547.

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28

Bochenek, Magdalena Ludmila. "Regulation of cell motility by ephrin-B2 signalling." Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492474.

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Ephrin ligands and their Eph receptor tyrosine kinases both are surface tethered proteins that control cell shape and movements through direct cell-cell contact. Their binding, and subsequent clustering, triggers bidirectional signalling pathways, with signals transduced from the receptor (forward) and the ligand (reverse), that regulate the behaviour of both Eph- and ephrin- expressing cells. Recent evidence suggests that reverse ephrin-B2 signalling controls endothelial cell sprout outgrowth and tip elongation, and smooth muscle cell shape changes and behaviour. In addition, misregulation of ephrin-B2 expression is observed in various tumour types and high expression of this ligand is correlated with increased tumour vascularisation and tendency to metastasise. To investigate how ephrin-B2 "reverse" signalling pathways direct changes during angiogenesis and how the expression level of ephrin ligands influences changes in cell behaviour and cell mot motility, I have used Human Umbilical Vein Endothelial Cells (HUVECs) overexpressing ephrin ligands as a model system.
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29

Khan, Taslima. "Isolation and functional analysis of Xenopus Ephrin-A3." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399711.

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30

Koch, William Tyler. "Elucidating Mechanisms of Canonical Wnt - ephrin-B Crosstalk." Thesis, West Virginia University, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10146608.

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Throughout development, canonical Wnt signaling contributes to the formation and maintenance of a wide array of cells, tissues, and organs. Dys-regulated Wnt signaling during embryonic development is implicated in developmental defects known as neurochristopathies, including craniofacial and heart defects, as well as defects in neural development. Due to its roles in stem cell maintenance and self-renewal, tissue homeostasis, and regeneration, aberrant Wnt signaling in adult tissues can result in various forms of cancer, including colorectal cancer, breast cancer, lung cancer, and gastro-intestinal cancer, among others. Dys-regulated Wnt signaling is also implicated in other pathologies including bone disease, and metabolic diseases, such as Type II diabetes. Our lab has previously identified a novel crosstalk between canonical Wnt signaling and ephrin signaling. Ephrin signaling occurs through the interaction of ephrin ligands and Eph receptor tyrosine kinases, and is bidirectional. Due to the roles of ephrin signaling in tissue development and maintenance, aberrant ephrin signaling is implicated in many diseases including bone remodeling diseases, diabetes, and cancer. The molecular mechanism of the crosstalk between canonical Wnt signaling and ephrin-B signaling remains unknown. β-catenin is a key intracellular effector of canonical Wnt signaling that transduces the signal to the nucleus, where β-catenin interacts with the TCF/LEF transcription factors and activates transcription of target genes. Due to its central role in transducing the canonical Wnt signal to the nucleus, we predict that ephrin-B signaling antagonizes canonical Wnt signaling by affecting the stability and/or sub-cellular localization of β-catenin, or the interaction between β-catenin and TCF/LEF transcription factors. By employing mouse ephrin-B constructs in human cell lines, we show that the canonical Wnt - ephrin-B crosstalk is conserved between frogs and mammals. We also found that ephrin-B antagonism of canonical Wnt signaling is likely independent of ubiquitin proteasome system (UPS)-mediated degradation of β-catenin. Furthermore, confocal immunofluorescence microscopy revealed that overexpression of ephrin-B in HEK293T cells treated with lithium chloride (LiCl) seems to promote membrane localization of β-catenin, particularly at the apical Z sections. These results suggests that re-localization of β-catenin to the cell membrane may contribute to the ephrin-B antagonism of canonical Wnt signaling.

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Poole, Richard James. "The roles and regulation of Eph/Ephrins during zebrafish somitogenesis." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408911.

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32

Knott, Laura. "Cooperation between GDNF/Ret and EphrinA/EphA4 signals for motor axon pathway selection in the limb." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-78380.

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33

McLauglin, Todd Robert. "The role of eph/ephrins in the development of retinotectal topography /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3031944.

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34

Gregory, L. G. L. "Eph-ephrin signalling in cell sorting and directional migration." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1318081/.

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An important problem in developmental biology is to understand how precise patterns of cell types are maintained during development. Eph receptor tyrosine kinases and ephrins have key roles in stabilising these patterns of cell organisation and segregation during development and can restrict the movement of cells by promoting cell repulsion. Previous work by Alexei Poliakov in the Wilkinson lab has shown that Eph-ephrin signalling leads to directional persistence of migration, and modelling suggests that this can contribute to cell segregation. In order to test experimentally the contribution of directional persistence in cell segregation, I have used and developed in vitro assays to dissect the roles of EphB2-ephrinB1 signalling in cell segregation, boundary sharpening and directional persistence. In these assays, stable HEK293 cell lines expressing EphB2 or ephrinB1 are mixed in cell culture and this leads to segregation of the two cell populations. Plating these cells either side of a removable barrier and allowing migration of cells towards each other leads to the formation of a sharp boundary on interaction. Analysis of cell behaviour shows EphB2 cells to move more persistently after interaction with ephrinB1 cells. To analyse how EphB2-ephrinB1 interactions lead to directional persistence of migration, my studies have focussed on the role of components potentially involved in directional persistence that act downstream of EphB2-ephrinB1 signalling, including the planar cell polarity (PCP) pathway (Dishevelled and Daam1) and core polarity components such as the PAR proteins (PAR-3 and PAR-6B). The PCP and PAR components were all found to have roles in cell segregation, as siRNA-mediated knockdown of each of these components disrupted EphB2-ephrinB1 mediated cell segregation and boundary sharpening. However, cell behaviour studies showed that only Dishevelled and PAR-6B have roles in EphB2-ephrinB1 mediated directional persistence, whilst Daam1 knockdown has no effect on the migratory response of cells. PAR-3 knockdown affects the basal ability of cells to migrate, potentially due to its role in establishing front-rear polarity. Taken together, these findings can be explained by a model in which Dishevelled and PAR-6B have a role in EphB2-ephrinB1 mediated directional persistence required for cell segregation and boundary sharpening. I propose that Daam1 may function in the contact inhibition of locomotion between cells also required for segregation.
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Harbott, Lene Karen. "Signalling pathways mediating ephrin-A-induced growth cone collapse." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446636/.

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The ephrin-A family of axon guidance cues, which activate the EphA family of receptor tyrosine kinases, guide the axons of many types of neuron to the correct target during embryonic development. One particularly well-studied example is the projection of RGC processes to precise positions in the midbrain target that reflect the position of the RGC in the retina. Ephrin-As are membrane-tethered molecules expressed in a gradient in the midbrain, and they govern the formation of the retinotectal map by differential, contact-mediated repulsion of Eph-A-expressing RGC axons. In order to identify signalling molecules that mediate ephrin-A induced repulsion of RGCs, I have developed a novel co-culture assay in which contact with a single non-neuronal cell that expresses endogenous levels of ephrin-A induces rapid loss of RGC growth cone lamella, followed by axon retraction. I have confirmed that these cellular responses are mediated by neuronal EphA receptor signalling and, in combination with the traditional soluble collapse assay, have used this physiologically relevant co-culture assay to identify a more specific role for the Rho effector ROCK in ephrin-A-induced RGC responses than has previously been published. Specifically ROCK activity mediates ephrin-A-induced RGC axon retraction, but not loss of growth cone lamella. I have also identified the non-receptor tyrosine kinase Abl as having a major role in the ephrin-A-induced RGC repulsive response, as the Abl kinase inhibitor STI571 prevents both the ephrin-A-induced loss of RGC lamella and axon retraction. I have demonstrated the existence of a protein complex containing active Eph receptors, Abl and Mena, and shown that disruption of this complex correlates with STI571-dependent inhibition of the ephrin-A-induced RGC repulsive responses. These results comprise the first evidence that Abl plays a role in mediating Eph receptor signals, and is involved in the cytoskeletal rearrangements that underlie ephrin-A-induced growth cone collapse in vitro, and thus both complement and extend the published evidence demonstrating a role for Abl in mediating axon guidance in vivo.
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Dickinson, Sarah. "Regulation of the actin cytoskeleton by ephrin-B signalling." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445415/.

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Ephrin ligands and their Eph receptors play an essential role in angiogenesis during development. Both ephrins and Eph receptors are membrane-tethered proteins and their interaction at sites of cell-cell contact triggers bi-directional signalling, with signals transduced from the receptor (forward signalling) and ligand (reverse signalling). I have used two model systems to study ephrin-B2 signalling: Swiss 3T3 fibroblasts expressing exogenous ephrin-B2 and Human Umbilical Arterial Endothelial Cells (HUAECs) endogenously expressing ephrin-Bs. Stimulation of ephrin-B2 with soluble EphB receptors, has enabled the characterisation of the cellular responses, and signalling pathways, triggered by ephrin-B2 activation. I have shown that clustering of expressed ephrin-B2 in cultured fibroblasts induces a loss of cell-cell contact, dependent on the presence of serum factors and independent of actin-myosin contractility. The intracellular domain of ephrin-B2 is essential: tyrosine phosphorylation of the ligand via Src, and binding of the adaptor protein Grb4 are required for loss of cell-cell contact. Stimulation of endogenous ephrin-B2 in cultured endothelial cells results in dramatic cell retraction, and in a proportion of cells membrane blebbing. I have shown that the small GTPase Rho and activation of its downstream effector ROCK are essential for membrane retraction to occur, which is driven by an actin-myosin contraction event. In addition, I find that the c-Jun amino terminal kinase (JNK) is required for retraction, acting upstream of Rho/ROCK, and retraction occurs independently of Grb4. The cell contraction response to ephrin-B2 activation is rapid and transient with cells recovering to re-spread lamellipodia within minutes. Re-spreading is coupled to a loss of actin stress fibres and concomitant with down regulation of Rho and ROCK activity.
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Ojima, Tomonari. "EphrinA1 inhibits vascular endothelial growth factor-induced intracellular signaling and suppresses retinal neovascularization and blood-retinal barrier breakdown." Kyoto University, 2006. http://hdl.handle.net/2433/143818.

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38

Göpel, Ulrike [Verfasser]. "Die Verteilung von ephrinB2 und EphB4 im Gewebe der adulten Maus / Ulrike Göpel." Köln : Deutsche Zentralbibliothek für Medizin, 2014. http://d-nb.info/1063171741/34.

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Liu, Hui [Verfasser], and Markus [Akademischer Betreuer] Hecker. "The role of EphB/ephrinB in inflammation / Hui Liu ; Betreuer: Markus Hecker." Heidelberg : Universitätsbibliothek Heidelberg, 2013. http://d-nb.info/1177809796/34.

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40

Wirnhier, Susanne. "Eph-Rezeptoren, Ephrine und Notch bei der Ausbildung von Gewebegrenzen in Hydra." Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-183773.

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41

Pfaff, Dennis. "EphB-ephrinB interactions controlling monocyte and tumor cell adhesion to endothelial cells." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:25-opus-50510.

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42

Genet, Gaël. "Ephrine-B1 : une nouvelle protéine structurante des membranes latérales des cardiomyocytes adultes." Toulouse 3, 2013. http://www.theses.fr/2013TOU30193.

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Ephrine-B1 est exprimée au niveau de la membrane latérale (ML) du cardiomyocyte (CM). Sa délétion (KO général et ciblé dans les CMs) entraine une désorganisation architecturale du tissu cardiaque, corrélée à une perte de la morphologie en brique du CM et de l'ultrastructure de la ML. Ces animaux démontrent une hypersensibilité au stress barométrique caractérisée par une mortalité élevée et une exacerbation de la désorganisation tissulaire. Dans un modèle d'insuffisance cardiaque (IC), l'expression génique d'éphrine-B1dans les CMs est diminuée de 50%. Ce travail suggère qu'éphrine-B1, en stabilisant la structure de la ML et la morphologie du CM, pourrait représenter un nouvel acteur participant à la mise en place de l'IC. Par l'utilisation de la Microscopie de Force Atomique nous avons montré que chez des souris saines, la surface du CM présente une architecture périodique en creux / crêtes ; les crêtes étant corrélées à la présence de mitochondries subsarcolemmales (SSM). Les CMs de souris présentant une IC post ischémiques présentent une désorganisation générale de la topographie de surface du sarcolemme caractérisée par une perte de la périodicité creux/crêtes. Ces modifications sont associées à une mort des SSM, rendant compte de surfaces lisses du CM. Un stress osmotique (formamide) indique que la mort des SSM précède la déstructuration des Tubules-T. Cette mort des SSM pourrait donc représenter un événement initiateur de l'évolution vers l'IC. L'étude du rôle d'éphrine-B1 dans la structuration du sarcolemme ouvre donc un nouvel axe de recherche et soulève l'importance des altérations de la ML des CMs dans l'apparition de l'IC
Ephrin-B1 is expressed at the lateral membrane (ML) of the cardiomyocyte (CM). Its deletion (KO General and targeted in CMs) causes an architectural disorganization of the heart tissue, correlated with a loss of the rode shape of CMs and ultrastructure of the ML. These animals show hypersensitivity to barometric stress characterized by high mortality and exacerbation of tissue disorganization. In a model of heart failure (HF), gene expression of ephrin - B1dans CMs is reduced by 50 %. This work suggests that Ephrine-B1, stabilizing the structure of the ML and morphology of CM could be a new player involved in the development of the HF. Using atomic force microscopy we have shown that in healthy mice, the surface of the CM has a periodic architecture hollow / crests, peaks are correlated to the presence of subsarcolemmal mitochondria (SSM). The CMs of mice with ischemic post HF have a general disorganization of the surface topography of the sarcolemma characterized by a loss of hollow / crests frequency. These changes are associated with death SSM, reporting CM smooth surfaces. Osmotic stress ( formamide ) indicates that the death of SSM before the breakdown of T - tubules. The death of SSM could therefore represent an initiating event of changes to the HF. The study of the ephrin -B1 role in structuring the sarcolemma thus opens a new research and raises the importance of alterations in the ML of CMs in the development of the HF
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43

Zarbalis, Konstantinos. "Molekulare und funktionale Analyse des Ephrin-A5-Gens der Maus." [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=960645179.

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44

Batson, Jennifer. "Regulation of contact inhibition of locomotion by Eph-ephrin signalling." Thesis, University of Bristol, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627947.

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Metastatic prostate cancer cells display EphB receptor-mediated attraction when they contact stromal fibroblasts but EphA-driven repulsion and contact inhibition of locomotion (CIL) when they contact one another. The impact of these social interactions between cells during cancer cell invasion and the signalling mechanisms downstream of Eph receptors are unclear. Here, I show that EphA receptors drive prostate cancer cell dissemination in a 20 dispersal assay and a 3D cancer cell" spheroid assay by activating repulsive interactions and CIL between contacting prostate cancer cells. I show that EphA receptors interact with the exchange factor Vav2 to activate RhoA, and that both Vav2 and RhoA are required for prostate cancer cell-cell repulsion. Using pharmacological inhibitors I show actomyosin contractility is not a key driver of CIL. I find instead that microtubule dynamics are important for generating the front-rear polarity switch required during CIL, and that EphA2/EphA4, Vav2 and RhoA affect microtubule stability in prostate cancer cells. Furthermore, I find that in EphA2/EphA4, Vav2 or RhoA knockdown cells, contact repulsion can be restored by partial microtubule destabilisation. I propose that EphAVav2- RhoA-mediated repulsion between contacting cancer cells at the tumour edge could enhance their local metastatic invasion and dissemination from the primary tumour. Subsequently, EphB-mediated attractive migration and failure of CIL, between prostate cancer cells contacting ephrin-B2· expressing fibroblasts, could facilitate cancer cell invasion through the surrounding stroma. Stimulation of prostate cancer cells with ephrin-B2lFc leads to filopodia formation and activation of Cdc42. I show that Cdc42-silenced PC-3 cells have significantly impaired migration towards surface coated ephrin-B2 compared with control siRNA-treated cells. Furthermore, Cdc42 is required for attractive migration and defective CIL during collisions b~tween advanced prostate cancer cells and ephrin-B2-expressing fibroblasts. Using organotypic 3D gel invasion assays, I show that ephrin-B2 expressing fibroblasts enhance prostate cancer cell invasion. These data suggest that EphB-Cdc42-mediated attractive interactions with fibroblasts and defective CIL might facilitate prostate cancer cell invasion through the surrounding stroma.
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45

Finkelmeier, Fabian [Verfasser]. "Die Rolle des Eph/Ephrin Systems bei Hirntumoren / Fabian Finkelmeier." Gießen : Universitätsbibliothek, 2011. http://d-nb.info/1063111358/34.

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46

Fero, Daniel James. "The role of PI3K in Ephrin-A1 induced cell retraction." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3315045.

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Thesis (Ph. D.)--University of California, San Diego, 2008.
Title from first page of PDF file (viewed August 4, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 104-113).
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47

Fujii, Haruko. "Eph-ephrin A system regulates murine blastocyst attachment and spreading." Kyoto University, 2010. http://hdl.handle.net/2433/97940.

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48

Fabes, J. "Investigating the role of ephrin signalling in spinal cord injury." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445432/.

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Spinal cord injury in adult mammals commonly leads to the permanent loss of motor and sensory function in regions of the body below the level of injury. The inability of the central nervous system to regenerate is, in part, due to the presence of growth-inhibitory agents surrounding the lesion site. This thesis presents a previously unreported, inhibitory interaction between ephrinB2 expressed on reactive astrocytes and the EphA4 receptor present on lesioned corticospinal tract axons. This interaction appears to mediate the unusually large retraction of the corticospinal tract away from spinal cord injury sites. An attempt to interfere with this interaction by implanting a cell line secreting the ephrinA5 receptor binding domain is reported. While this approach induced improvements in regenerative sprouting from the corticospinal tract, complications with immune rejection and cell proliferation stopped further investigation. A second intervention using a small peptide with high affinity and specificity for the EphA4 receptor is also reported. Intrathecal infusion of this peptide for 14 or 28 days after injury reversed the retraction of the corticospinal tract and induced improvements in regenerative sprouting from corticospinal and rubrospinal tracts following dorsal or lateral white matter transection injuries. Sprouts were seen to migrate long distances, often to the astrocyte margin of the lesion cavity. Astrocyte behaviour following injury was also altered with the formation of astrocytic 'bridges' into the lesion cavity along which regenerating axons grew. Functional recovery was also enhanced with improvements in the paw reaching assay within 10 days of a unilateral dorsal column lesion with a 30% recovery of function at 28 days post-operation. The simplicity of this intervention and direct translation to human application make it a promising candidate for use in combinatorial approaches to human spinal cord injury treatment.
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Hirsch, Karmela [Verfasser]. "Expression von Ephrin-Rezeptoren und Ephrin-Liganden in mit Ammoniak behandelten, kultivierten Rattenastrozyten und in post mortem Hirnproben von Leberzirrhosepatienten mit hepatischer Enzephalopathie / Karmela Hirsch." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2019. http://d-nb.info/1180023609/34.

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50

Depaepe, Vanessa. "Détermination par approche transgénique du rôle de gênes de guidance axonale, les éphrines, dans le développement du néocortex cérébral." Doctoral thesis, Universite Libre de Bruxelles, 2005. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210986.

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Les ephrines et leurs récepteurs Eph constituent une famille multigénique de facteurs de guidage cellulaire et axonal. Ces facteurs jouent un rôle-clé dans l’établissement de cartes neurales topographiques, notamment au niveau des connexions thalamocorticales, réseau neuronal majeur du cerveau des mammifères.

Notre projet visait initialement à étudier l’implication des ephrines corticales dans la génèse des connexions thalamocorticales par une approche de gain de fonction. Pour ce faire, nous avons généré des souris transgéniques présentant une expression ectopique spécifique de l’ephrine-A5 dans le cortex en développement, en utilisant une technique de transgénèse d’addition par chromosome artificiel de bactéries (BAC).

De façon surprenante, l’analyse de ces souris nous a révélé que les ephrines, à côté de leurs rôles classiques de facteurs de guidage, influençaient la taille du cortex cérébral en régulant l’apoptose des progéniteurs neuronaux. En effet, nous avons pu montrer que l’expression ectopique du ligand ephrine-A5 par les progéniteurs corticaux exprimant son récepteur EphA7 résultait en une déplétion précoce en progéniteurs corticaux par apoptose, et une diminution subséquente de la taille du cortex. Cette vague apoptotique est observée en l’absence de toute altération détectable de la prolifération, la différenciation et la migration neurale dans le cortex.

Nous avons étayé notre étude in vivo par des expériences in vitro, qui ont montré que l’ephrine-A5 recombinante était capable d’induire rapidement la mort des progéniteurs neuronaux dissociés. Nous avons également montré que cette mort cellulaire impliquait l’activation de la caspase-3, confirmant ainsi l’effet direct des ephrines et de leurs récepteurs sur une ou plusieurs cascades apoptotiques. Par contre, la stimulation des neurones post-mitotiques corticaux par l’ephrine-A5 est accompagnée d’une activation de la caspase-3 sans mort cellulaire apparente. La signalisation ephrine/Eph induirait donc l’activation de la caspase-3 dans différents types cellulaires, sans que celle-ci ne soit systématiquement le reflet d’une mort cellulaire programmée.

Parallèlement, afin d’évaluer l’importance physiologique de cette voie pro-apoptotique dépendante des ephrines, nous avons étudié des souris présentant une perte de fonction du récepteur EphA7. L’analyse de ces mutants nous a permis de mettre en évidence une diminution de l’apoptose des progéniteurs corticaux, une augmentation de la taille du cortex, ainsi qu’une hypercroissance exencéphalique de tout le cerveau antérieur dans les cas les plus extrêmes. Ces observations indiquent donc que les ephrines sont nécessaires au contrôle de la mort cellulaire programmée des progéniteurs du cortex cérébral. Nous avons également observé le même phénotype exencéphalique dans des mutants déficients en ephrines-A2, -A3 et -A5, dont l’analyse préliminaire suggère également des défauts de processus apoptotiques.

Nos diverses expériences, combinant une approche par gain et perte de fonction, à la fois in vivo et in vitro, ont ainsi permis de proposer un nouveau rôle des ephrines en marge de leur implication dans la guidance axonale, à savoir un rôle dans le contrôle de la taille cérébrale par induction de l’apoptose des progéniteurs corticaux.

La mise en évidence de cette nouvelle voie de signalisation pro-apoptotique pourrait avoir des implications importantes dans d’autres aspects de la biologie du développement et des cellules souches, ainsi que dans l’oncogénèse.


Doctorat en sciences biomédicales
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