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Your search keyword '"Fondation pour le Recherche Medicale"' showing total 4 results
Start Over Author "Fondation pour le Recherche Medicale" Topic 0302 clinical medicine
4 results on '"Fondation pour le Recherche Medicale"'

1. In vivo assembly of the axon initial segment in motor neurons

Author

Masayuki Komada, François Couraud, Barbara Le Bras, Antonny Czarnecki, Amélie Fréal, Pascal Legendre, Peter J. Brophy, Marc Davenne, Erika Bullier, Développement de l'organisation spinale = Development of the spinal cord organization (NPS-10), Neuroscience Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Association Francaise contre les Myopathies (AFM), Fondation pour le Recherche Medicale (FRM), Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC), Neurosciences Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Ankyrins, Histology, Neuroscience(all), Population, Action Potentials, Biology, Development, Axonogenesis, Mice, 03 medical and health sciences, 0302 clinical medicine, AnkyrinG, medicine, Animals, Ankyrin, Spectrin, Nerve Growth Factors, Axon, education, 030304 developmental biology, Mice, Knockout, Motor Neurons, chemistry.chemical_classification, 0303 health sciences, education.field_of_study, General Neuroscience, Sodium channel, Axon initial segment, Axons, Nerve growth factor, medicine.anatomical_structure, nervous system, chemistry, Original Article, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Anatomy, Cell Adhesion Molecules, Neuroscience, 030217 neurology & neurosurgery
Abstract

The axon initial segment (AIS) is responsible for both the modulation of action potentials and the maintenance of neuronal polarity. Yet, the molecular mechanisms controlling its assembly are incompletely understood. Our study in single electroporated motor neurons in mouse embryos revealed that AnkyrinG (AnkG), the AIS master organizer, is undetectable in bipolar migrating motor neurons, but is already expressed at the beginning of axonogenesis at E9.5 and initially distributed homogeneously along the entire growing axon. Then, from E11.5, a stage when AnkG is already apposed to the membrane, as observed by electron microscopy, the protein progressively becomes restricted to the proximal axon. Analysis on the global motor neurons population indicated that Neurofascin follows an identical spatio-temporal distribution, whereas sodium channels and β4-spectrin only appear along AnkG+ segments at E11.5. Early patch-clamp recordings of individual motor neurons indicated that at E12.5 these nascent AISs are already able to generate spikes. Using knock-out mice, we demonstrated that neither β4-spectrin nor Neurofascin control the distal-to-proximal restriction of AnkG. Electronic supplementary material The online version of this article (doi:10.1007/s00429-013-0578-7) contains supplementary material, which is available to authorized users.

Published
2014
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2. An APOA5 3' UTR variant associated with plasma triglycerides triggers APOA5 downregulation by creating a functional miR-485-5p binding site

Author

Sophie Rome, Cyrielle Caussy, Vanessa Euthine, Mathilde Di Filippo, Sybil Charrière, Etienne Lefai, Agnès Sassolas, Philippe Moulin, C. Marcais, Mireille Delay, Audrey Jalabert, Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN), Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-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)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Institut National de la Recherche Agronomique (INRA), Societe Francaise d'Endocrinologie, Institut National de la Sante et de la Recherche Medicale, Universite Claude Bernard Lyon 1, Fondation pour le Recherche Medicale, Fondation de France, Institut National de la Recherche Agronomique (INRA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), and Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hospices Civils de Lyon (HCL)

Subjects
Untranslated region, Liver/metabolism, [SDV]Life Sciences [q-bio], Down-Regulation, MiRNA binding, Apolipoproteins A/*genetics/metabolism, 030204 cardiovascular system & hematology, Biology, Luciferases/metabolism, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, Report, microRNA, Genetics, Humans, Genetics(clinical), Luciferase, Triglycerides/*blood, Allele, Binding site, Luciferases, 3' Untranslated Regions, Apolipoproteins A, Triglycerides, Genetics (clinical), Alleles, 030304 developmental biology, 0303 health sciences, Binding Sites, HEK 293 cells, 3' Untranslated Regions/*genetics, Genetic Variation, Computational Biology, MicroRNAs/*genetics/metabolism, Molecular biology, MicroRNAs, HEK293 Cells, Liver, Haplotypes, Apolipoprotein A-V
Abstract

International audience; APOA5 c.*158C\textgreaterT (rs2266788), located in the 3' UTR, belongs to APOA5 haplotype 2 (APOA5*2), which is strongly associated with plasma triglyceride levels and modulates the occurrence of both moderate and severe hypertriglyceridemia. Individuals with APOA5*2 display reduced APOA5 expression at the posttranscriptional level. However, the functionality of this haplotype remains unclear. We hypothesized that the hypertriglyceridemic effects of APOA5*2 could involve miRNA regulation in the APOA5 3' UTR. Bioinformatic studies have identified the creation of a potential miRNA binding site for liver-expressed miR-485-5p (MIRN485-5p) in the mutant APOA5 3' UTR with the c.*158C allele. In human embryonic kidney 293T (HEK293T) cells cotransfected with an APOA5 3' UTR luciferase reporter vector and a miR485-5p precursor, c.*158C allele expression was significantly decreased. Moreover, in HuH-7 cells endogenously expressing miR-485-5p, we observed that luciferase activity was significantly lower in the presence of the c.*158C allele than in the presence of the c.*158T allele, which was completely reversed by a miR-485-5p inhibitor. We demonstrated that the rare c.*158C APOA5 allele creates a functional target site for liver-expressed miR-485-5p. Therefore, we propose that the well-documented hypertriglyceridemic effect of APOA5*2 involves an APOA5 posttranscriptional downregulation mediated by miR-485-5p.

Published
2014
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3. The overexpression of the putative gut stem cell marker Musashi-1 induces tumorigenesis through Wnt and Notch activation

Author

Colette Roche, Amélie Rezza, Seham Skah, Jacques Samarut, Julien Nadjar, Michelina Plateroti, ProdInra, Migration, Institut de Génomique Fonctionnelle de Lyon (IGFL), École normale supérieure - Lyon (ENS Lyon)-Institut National de la Recherche Agronomique (INRA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), U-865, Institut National de la Santé et de la Recherche Médicale (INSERM), Agence Nationale pour la Recherche ( ANR-06-BLAN-0232-01), Institut National du Cancer (INCA-2007-Col6), Ligue Nationale contre le Cancer, Fondation pour le Recherche Medicale, Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Recherche Agronomique (INRA)-École normale supérieure - Lyon (ENS Lyon), and École normale supérieure de Lyon (ENS de Lyon)-Institut National de la Recherche Agronomique (INRA)-Université Claude Bernard Lyon 1 (UCBL)

Subjects
[SDV]Life Sciences [q-bio], Intestinal tumorigenesis, Stem cells, Stem cell marker, thyroid-hormone, Mice, 0302 clinical medicine, rna, Transgenes, Intestinal Mucosa, Cell Line, Transformed, 0303 health sciences, Receptors, Notch, Wnt signaling pathway, LRP6, RNA-Binding Proteins, LRP5, progenitor cells, Intestinal epithelium, binding protein musashi-1, [SDV] Life Sciences [q-bio], Cell Transformation, Neoplastic, 030220 oncology & carcinogenesis, Stem cell, translational repression, Transcriptional Activation, Transplantation, Heterologous, Nerve Tissue Proteins, Biology, [INFO] Computer Science [cs], 03 medical and health sciences, Wnt, expression, Animals, [INFO]Computer Science [cs], Progenitor cell, gene, alpha tr-alpha, mouse, 030304 developmental biology, Cell Proliferation, Cell Biology, Mice, Mutant Strains, Rats, Wnt Proteins, Animals, Newborn, Musashi-1, Cell culture, Cancer research, intestinal epithelial-cells, Biomarkers
Abstract

International audience; The RNA-binding protein Musashi-1 (Msi1) has been proposed as a marker of intestinal epithelial stem cells. These cells are responsible for the continuous renewal of the intestinal epithelium. Although the function of Msi1 has been studied in several organs from different species and in mammalian cell lines, its function and molecular regulation in mouse intestinal epithelium progenitor cells are still undefined. We describe here that, in these cells, the expression of Msi1 is regulated by the canonical Wnt pathway, through a mechanism involving a functional Tcf/Lef binding site on its promoter. An in vitro study in intestinal epithelium primary cultures showed that Msi1 overexpression promotes progenitor proliferation and activates Wnt and Notch pathways. Moreover, Msi1-overexpressing cells exhibit tumorigenic properties in xenograft experiments. These data point to a positive feedback loop between Msi1 and Wnt in intestinal epithelial progenitors. They also suggest that Msi1 has oncogenic properties in these cells, probably through induction of both the Wnt and Notch pathways.

Published
2010
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4. Membrane Lipids Tune Synaptic Transmission by Direct Modulation of Presynaptic Potassium Channels

Author

Christophe Mulle, Mario Carta, Joana Lourenço, Silvia Viana DaSilva, Nelson Rebola, Zsolt Szabo, Christophe Blanchet, Carsten Schultz, André Nadler, Agathe Verraes, Frederic Lanore, Indisciplinary Institute for Neuroscience, UMR 5297, Institut Jacques Monod (IJM (UMR_7592)), Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), INSERM ERL U950, Membrane Traffic in Neuronal and Epithelial Morphogenesis, Institut National de la Santé et de la Recherche Médicale (INSERM), European Molecular Biology Laboratory [Heidelberg] (EMBL), and EIF Fellowship (project name KARTRAF), SYNSCAFF, the Conseil Regional of Aquitaine, the Fondation pour le Recherche Medicale, VANR ASD/LD, Dalhousie University, ESF EuroMembrane program (TraPPs)

Subjects
MESH: Hippocampus, Potassium Channels, Long-Term Potentiation, MESH: Neurons, Gating, Hippocampus, Synaptic Transmission, MESH: Synapses, Mice, 0302 clinical medicine, Postsynaptic potential, MESH: Animals, Neurons, 0303 health sciences, Chemistry, General Neuroscience, Pyramidal Cells, MESH: Electric Stimulation, Long-term potentiation, MESH: Potassium Channels, Potassium channel, medicine.anatomical_structure, Modulation, Mossy Fibers, Hippocampal, Excitatory postsynaptic potential, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Membrane lipids, Neuroscience(all), Neurotransmission, Biology, 03 medical and health sciences, Membrane Lipids, MESH: Long-Term Potentiation, MESH: Mice, Inbred C57BL, medicine, MESH: Synaptic Transmission, Animals, MESH: Excitatory Postsynaptic Potentials, MESH: Mice, 030304 developmental biology, Post-tetanic potentiation, MESH: Mossy Fibers, Hippocampal, Excitatory Postsynaptic Potentials, MESH: Pyramidal Cells, Electric Stimulation, Mice, Inbred C57BL, Synaptic plasticity, Synapses, Biophysics, Retrograde signaling, Neuron, MESH: Membrane Lipids, Neuroscience, 030217 neurology & neurosurgery
Abstract

International audience; Voltage-gated potassium (Kv) channels are involved in action potential (AP) repolarization in excitable cells. Exogenous application of membrane-derived lipids, such as arachidonic acid (AA), regulates the gating of Kv channels. Whether membrane-derived lipids released under physiological conditions have an impact on neuronal coding through this mechanism is unknown. We show that AA released in an activity-dependent manner from postsynaptic hippocampal CA3 pyramidal cells acts as retrograde messenger, inducing a robust facilitation of mossy fiber (Mf) synaptic transmission over several minutes. AA acts by broadening presynaptic APs through the direct modulation of Kv channels. This form of short-term plasticity can be triggered when postsynaptic cell fires with physiologically relevant patterns and sets the threshold for the induction of the presynaptic form of long-term potentiation (LTP) at hippocampal Mf synapses. Hence, direct modulation of presynaptic Kv channels by activity-dependent release of lipids serves as a physiological mechanism for tuning synaptic transmission.

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