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4. Switching of RNA splicing regulators in immature neuroblasts: a key step in adult neurogenesis

Author

Bernou, Corentin, primary, Mouthon, Marc-André, additional, Daynac, Mathieu, additional, Kortulewski, Thierry, additional, Demaille, Benjamin, additional, Barroca, Vilma, additional, Couillard-Despres, Sébastien, additional, Dechamps, Nathalie, additional, Ménard, Véronique, additional, Bellenger, Léa, additional, Antoniewski, Christophe, additional, Chicheportiche, Alexandra, additional, and Boussin, François D., additional

Published
2024
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5. Author Response: Switching of RNA splicing regulators in immature neuroblasts: a key step in adult neurogenesis

Author

Bernou, Corentin, primary, Mouthon, Marc-André, additional, Daynac, Mathieu, additional, Kortulewski, Thierry, additional, Demaille, Benjamin, additional, Barroca, Vilma, additional, Couillard-Despres, Sébastien, additional, Dechamps, Nathalie, additional, Ménard, Véronique, additional, Bellenger, Léa, additional, Antoniewski, Christophe, additional, Chicheportiche, Alexandra, additional, and Boussin, François D., additional

Published
2024
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6. Evidence of the ability of endocrine disrupting compounds to induce testicular germ cell cancer in humans

Author

Nicolas, Nour, primary, Moison, Delphine, additional, Jampy, Amandine, additional, Masson, Quentin, additional, Dechamps, Nathalie, additional, Messiaen, Sébastien, additional, Abdallah, Sonia, additional, Pozzi-Gaudin, Stéphanie, additional, Benachi, Alexandra, additional, Ulveling, Damien, additional, Francastel, Claire, additional, Rouiller-Fabre, Virginie, additional, Livera, Gabriel, additional, and Guerquin, Marie-Justine, additional

Published
2023
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8. Switching of RNA splicing regulators in immature neuroblasts: a key step in adult neurogenesis

Author

Bernou, Corentin, primary, Mouthon, Marc-André, additional, Daynac, Mathieu, additional, Demaille, Benjamin, additional, Barroca, Vilma, additional, Couillard-Despres, Sébastien, additional, Dechamps, Nathalie, additional, Ménard, Véronique, additional, Bellenger, Léa, additional, Antoniewski, Christophe, additional, Chicheportiche, Alexandra, additional, and D. Boussin, François, additional

Published
2023
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9. Loss of CD24 promotes radiation‑ and chemo‑resistance by inducing stemness properties associated with a hybrid E/M state in breast cancer cells

Author

Bontemps, Isaline, primary, Lallemand, Celine, additional, Biard, Denis, additional, Dechamps, Nathalie, additional, Kortulewski, Thierry, additional, Bourneuf, Emmanuelle, additional, Siberchicot, Capucine, additional, Boussin, François, additional, Chevillard, Sylvie, additional, Campalans, Anna, additional, and Lebeau, Jerome, additional

Published
2022
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10. Modulation of astrocyte reactivity improves functional deficits in mouse models of Alzheimer’s disease

Author

Ceyzériat, Kelly, Ben Haim, Lucile, Denizot, Audrey, Pommier, Dylan, Matos, Marco, Guillemaud, Océane, Palomares, Marie-Ange, Abjean, Laurene, Petit, Fanny, Gipchtein, Pauline, Gaillard, Marie-Claude, Guillermier, Martine, Bernier, Sueva, Gaudin, Mylène, Auregan, Gwenaëlle, Joséphine, Charlène, Dechamps, Nathalie, Veran, Julien, Langlais, Valentin, Cambon, Karine, Bemelmans, Alexis-Pierre, Baijer, Jan, Bonvento, Gilles, Dhenain, Marc, Deleuze, Jean-François, Oliet, Stéphane, Brouillet, Emmanuel, Hantraye, Philippe, Carrillo-de Sauvage, Maria-Angeles, Olaso, Robert, Panatier, Aude, Escartin, Carole, Laboratoire des Maladies Neurodégénératives - UMR 9199 (LMN), Service MIRCEN (MIRCEN), Université Paris-Saclay-Institut de Biologie François JACOB (JACOB), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Institut de Biologie François JACOB (JACOB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Sud - Paris 11 (UP11)-Centre National de la Recherche Scientifique (CNRS), Artificial Evolution and Computational Biology (BEAGLE), Laboratoire d'InfoRmatique en Image et Systèmes d'information (LIRIS), Université Lumière - Lyon 2 (UL2)-École Centrale de Lyon (ECL), Université de Lyon-Université de Lyon-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Université Lumière - Lyon 2 (UL2)-École Centrale de Lyon (ECL), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Inria Grenoble - Rhône-Alpes, Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria)-Laboratoire de Biométrie et Biologie Evolutive - UMR 5558 (LBBE), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de Recherche en Informatique et en Automatique (Inria)-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Centre National de la Recherche Scientifique (CNRS)-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Centre National de la Recherche Scientifique (CNRS), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Cellules Souches et Radiations (SCSR (U967 / UMR-E_008)), Université Paris-Sud - Paris 11 (UP11)-Université Paris Diderot - Paris 7 (UPD7)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Neurocentre Magendie-U862, Institut François Magendie, and Université de Bordeaux, Institut National de la Santé et de la Recherche Médicale (INSERM), Division of Reproductive Biology, Stanford University [Stanford], CEA [Fontenay-aux-Roses] (UGRA / SETA), Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Sanofi-Aventis, Centre for Reserach in Neuroscience, McGill University-Montreal General Hospital, McGill University Health Center [Montreal] (MUHC)-McGill University Health Center [Montreal] (MUHC), Centre National de Génotypage (CNG), Institut François Magendie, Institut de Biologie François JACOB (JACOB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-École Centrale de Lyon (ECL), Université de Lyon-Université Lumière - Lyon 2 (UL2)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Université Lumière - Lyon 2 (UL2)-Inria Grenoble - Rhône-Alpes, Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, Stabilité génétique, Cellules Souches et Radiations (SCSR (U_967)), Université Paris-Sud - Paris 11 (UP11)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Department of Obstetrics and Gynecology [Stanford], Stanford Medicine, Stanford University-Stanford University, McGill University = Université McGill [Montréal, Canada]-Montreal General Hospital, Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie François JACOB (JACOB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie François JACOB (JACOB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Neurocentre Magendie : Physiopathologie de la Plasticité Neuronale (U1215 Inserm - UB), Université de Bordeaux (UB)-Institut François Magendie-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de Recherche en Génomique Humaine (CNRGH), Université Paris-Sud, UMR 967, Fontenay-aux-Roses, France, ANR-16-TERC-0016,DecodAstro,Decoder la complexité de la réactivité astrocytaire dans les maladies neurodégénératives(2016), ANR-11-INBS-0011,NeurATRIS,Infrastructure de Recherche Translationnelle pour les Biothérapies en Neurosciences(2011), ANR-10-LABX-0013,GENMED,Medical Genomics(2010), ANR-10-JCJC-1402,ACTIVASTRO,Modulation sélective des astrocytes activés : Suivi in situ par résonance magnétique et contribution à la mort neuronale dans la maladie de Huntington(2010), ANR-11-BSV4-0021,AstroConSyn,Contrôle de la transmission synaptique par la connexine 30 astrogliale: bases moléculaires et impact sur l'activité de réseau pathologique(2011), Centre National de la Recherche Scientifique (CNRS)-Service MIRCEN (MIRCEN), INSERM, Neurocentre Magendie, U1215, Physiopathologie de la Plasticité Neuronale, F-33000 Bordeaux, France, cambon, karine, Decoder la complexité de la réactivité astrocytaire dans les maladies neurodégénératives - - DecodAstro2016 - ANR-16-TERC-0016 - TERC - VALID, Infrastructures - Infrastructure de Recherche Translationnelle pour les Biothérapies en Neurosciences - - NeurATRIS2011 - ANR-11-INBS-0011 - INBS - VALID, Medical Genomics - - GENMED2010 - ANR-10-LABX-0013 - LABX - VALID, Jeunes Chercheuses et Jeunes Chercheurs - Modulation sélective des astrocytes activés : Suivi in situ par résonance magnétique et contribution à la mort neuronale dans la maladie de Huntington - - ACTIVASTRO2010 - ANR-10-JCJC-1402 - JCJC - VALID, and BLANC - Contrôle de la transmission synaptique par la connexine 30 astrogliale: bases moléculaires et impact sur l'activité de réseau pathologique - - AstroConSyn2011 - ANR-11-BSV4-0021 - BLANC - VALID

Subjects
Male, Viral vectors, JAK2-STAT3 pathway, [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Mice, Transgenic, Mouse models, Hippocampus, lcsh:RC346-429, Amyloid beta-Protein Precursor, Mice, Apolipoproteins E, Neuroinflammation, Alzheimer Disease, Glial Fibrillary Acidic Protein, Presenilin-1, Animals, Aspartic Acid Endopeptidases, Extracellular Signal-Regulated MAP Kinases, Maze Learning, lcsh:Neurology. Diseases of the nervous system, ComputingMilieux_MISCELLANEOUS, Amyloid beta-Peptides, Research, [SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Excitatory Postsynaptic Potentials, Signaling cascades, Janus Kinase 2, Disease Models, Animal, STAT1 Transcription Factor, Suppressor of Cytokine Signaling 3 Protein, Astrocytes, Mutation, Reactive astrocytes, Amyloid Precursor Protein Secretases, Alzheimer’s disease
Abstract

Astrocyte reactivity and neuroinflammation are hallmarks of CNS pathological conditions such as Alzheimer’s disease. However, the specific role of reactive astrocytes is still debated. This controversy may stem from the fact that most strategies used to modulate astrocyte reactivity and explore its contribution to disease outcomes have only limited specificity. Moreover, reactive astrocytes are now emerging as heterogeneous cells and all types of astrocyte reactivity may not be controlled efficiently by such strategies. Here, we used cell type-specific approaches in vivo and identified the JAK2-STAT3 pathway, as necessary and sufficient for the induction and maintenance of astrocyte reactivity. Modulation of this cascade by viral gene transfer in mouse astrocytes efficiently controlled several morphological and molecular features of reactivity. Inhibition of this pathway in mouse models of Alzheimer’s disease improved three key pathological hallmarks by reducing amyloid deposition, improving spatial learning and restoring synaptic deficits. In conclusion, the JAK2-STAT3 cascade operates as a master regulator of astrocyte reactivity in vivo. Its inhibition offers new therapeutic opportunities for Alzheimer’s disease. Electronic supplementary material The online version of this article (10.1186/s40478-018-0606-1) contains supplementary material, which is available to authorized users.

Published
2018
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11. Establishment and Characterization of a Reliable Xenograft Model of Hodgkin Lymphoma Suitable for the Study of Tumor Origin and the Design of New Therapies

Author

M’kacher, Radhia, primary, Frenzel, Monika, additional, Al Jawhari, Mustafa, additional, Junker, Steffen, additional, Cuceu, Corina, additional, Morat, Luc, additional, Bauchet, Anne-Laure, additional, Stimmer, Lev, additional, Lenain, Aude, additional, Dechamps, Nathalie, additional, Hempel, William, additional, Pottier, Geraldine, additional, Heidingsfelder, Leonhard, additional, Laplagne, Eric, additional, Borie, Claire, additional, Oudrhiri, Noufissa, additional, Jouni, Dima, additional, Bennaceur-Griscelli, Annelise, additional, Colicchio, Bruno, additional, Dieterlen, Alain, additional, Girinsky, Theodore, additional, Boisgard, Raphael, additional, Bourhis, Jean, additional, Bosq, Jacques, additional, Mehrling, Thomas, additional, Jeandidier, Eric, additional, and Carde, Patrice, additional

Published
2018
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15. Establishment and Characterization of a Reliable Xenograft Model of Hodgkin Lymphoma Suitable for the Study of Tumor Origin and the Design of New Therapies.

Author

M'kacher, Radhia, Frenzel, Monika, Al Jawhari, Mustafa, Junker, Steffen, Cuceu, Corina, Morat, Luc, Bauchet, Anne-Laure, Stimmer, Lev, Lenain, Aude, Dechamps, Nathalie, Hempel, William M., Pottier, Geraldine, Heidingsfelder, Leonhard, Laplagne, Eric, Borie, Claire, Oudrhiri, Noufissa, Jouni, Dima, Bennaceur-Griscelli, Annelise, Colicchio, Bruno, and Dieterlen, Alain

Subjects
TRANSFERASES, ANIMAL experimentation, BIOLOGICAL models, CELL lines, CYTOGENETICS, ENZYME inhibitors, FLOW cytometry, HISTONES, IMMUNOHISTOCHEMISTRY, LYMPHOCYTES, HODGKIN'S disease, MICE, GENETIC mutation, TELOMERES, XENOGRAFTS, PHENOTYPES, IN vitro studies, IN vivo studies, PHARMACODYNAMICS, GENETICS, DIAGNOSIS, PROGNOSIS, PHYSIOLOGY, THERAPEUTICS
Abstract

To identify the cells responsible for the initiation and maintenance of Hodgkin lymphoma (HL) cells, we have characterized a subpopulation of HL cells grown in vitro and in vivo with the aim of establishing a reliable and robust animal model for HL. To validate our model, we challenged the tumor cells in vivo by injecting the alkylating histone-deacetylase inhibitor, EDO-S101, a salvage regimen for HL patients, into xenografted mice. Methodology: Blood lymphocytes from 50 HL patients and seven HL cell lines were used. Immunohistochemistry, flow cytometry, and cytogenetics analyses were performed. The in vitro and in vivo effects of EDO-S101 were assessed. Results: We have successfully determined conditions for in vitro amplification and characterization of the HL L428-c subline, containing a higher proportion of CD30−/CD15− cells than the parental L428 cell line. This subline displayed excellent clonogenic potential and reliable reproducibility upon xenografting into immunodeficient NOD-SCID-gamma (−/−)(NSG) mice. Using cell sorting, we demonstrate that CD30−/CD15− subpopulations can gain the phenotype of the L428-c cell line in vitro. Moreover, the human cells recovered from the seventh week after injection of L428-c cells into NSG mice were small cells characterized by a high frequency of CD30−/CD15− cells. Cytogenetic analysis demonstrated that they were diploid and showed high telomere instability and telomerase activity. Accordingly, chromosomal instability emerged, as shown by the formation of dicentric chromosomes, ring chromosomes, and breakage/fusion/bridge cycles. Similarly, high telomerase activity and telomere instability were detected in circulating lymphocytes from HL patients. The beneficial effect of the histone-deacetylase inhibitor EDO-S101 as an anti-tumor drug validated our animal model. Conclusion: Our HL animal model requires only 103 cells and is characterized by a high survival/toxicity ratio and high reproducibility. Moreover, the cells that engraft in mice are characterized by a high frequency of small CD30−/CD15− cells exhibiting high telomerase activity and telomere dysfunction. [ABSTRACT FROM AUTHOR]

Published
2018
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