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4 results on '"Corinne Bachelin"'

1. Slit1 Protein Regulates SVZ-Derived Precursor Mobilization in the Adult Demyelinated CNS

Author

C Caillava, Corinne Bachelin, B Garcia-Diaz, A Baron-Van Evercooren, Nadège Sarrazin, G Spigoni, Alain Chédotal, Athena R. Ypsilanti, Cyrille Deboux, Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Institut de la Vision, Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Gestionnaire, Hal Sorbonne Université, Institut du Cerveau = Paris Brain Institute (ICM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)

Subjects
0301 basic medicine, neural precursor, CNS demyelination, animal diseases, [SDV]Life Sciences [q-bio], oligodendrocytes, Biology, Corpus callosum, migration, lcsh:RC321-571, Lesion, OLIG2, 03 medical and health sciences, Cellular and Molecular Neuroscience, Myelin, 0302 clinical medicine, Slit1, medicine, otorhinolaryngologic diseases, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Original Research, Neurogenesis, Oligodendrocyte, Cell biology, [SDV] Life Sciences [q-bio], stomatognathic diseases, myelin, 030104 developmental biology, medicine.anatomical_structure, nervous system, recruitment, Axon guidance, medicine.symptom, 030217 neurology & neurosurgery, Neuroscience
Abstract

International audience; Slit1 is a secreted axon guidance molecule, also involved in adult neurogenesis. In physiological conditions, Slit1 loss promotes ectopic dispersal of SVZ-derived neural precursors (SVZ-NPCs) into periventricular structures such as the corpus callosum. Demyelination of the corpus callosum triggers SVZ-NPC migration to ectopic locations and their recruitment by the lesion, suggesting a possible role for Slit1 in SVZ-NPCs ectopic dispersal regulation in pathological conditions. Here, we have investigated the function of Slit1 protein in the recruitment of SVZ-NPCs after CNS demyelination. We find that the dynamics of oligodendrogenesis and temporal profile of developmental myelination in Slit1 -/- mice are similar to Slit1 +/- controls. SVZ micro-dissection and RT-PCR from wild-type mice, show that Slits and Robos are physiologically regulated at the transcriptional level in response to corpus callosum demyelination suggesting their role in the process of SVZ-NPC ectopic migration in demyelinating conditions. Moreover, we find that the number of SVZ-NPCs recruited by the lesion increases in Sli1-/- mice compared to Slit1 +/- mice, leading to higher numbers of Olig2+ cells within the lesion. Time-lapse video-microscopy of immuno-purified NPCs shows that Slit1-deficient cells migrate faster and make more frequent directional changes than control NPCs, supporting a cell-autonomous mechanism of action of Slit1 in NPC migration. In conclusion, while Slit1 does not affect the normal developmental process of oligodendrogenesis and myelination, it regulates adult SVZ-NPC ectopic migration in response to demyelination, and consequently oligodendrocyte renewal within the lesion.

Published
2020
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2. The intellectual disability protein PAK3 regulates oligodendrocyte precursor cell differentiation

Author

Brahim Nait Oumesmar, Corinne Bachelin, Isabelle Dusart, Rosine Wehrlé, Majistor Raj Luxman Maglorius Renkilaraj, Lamia Bouslama-Oueghlani, Mohamed Doulazmi, Vidjeacoumary Cannaya, Zhengping Jia, Claire M. Wells, Lucas Baudouin, Jean-Vianney Barnier, Développement et plasticité des réseaux neuronaux = Development and Plasticity of Neural Networks (NPS-14), Neuroscience Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-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)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-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)-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)-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), and Neurosciences Paris Seine (NPS)

Subjects
Male, 0301 basic medicine, Intellectual disability, Anterior commissure, Biology, Corpus Callosum, lcsh:RC321-571, White matter, 03 medical and health sciences, Myelin, 0302 clinical medicine, Neural Stem Cells, Cell Movement, medicine, Animals, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Anterior Commissure, Brain, Cells, Cultured, Mice, Knockout, Kinase, Wild type, Oligodendrocyte differentiation, Cell Differentiation, White Matter, Oligodendrocyte, Cell biology, Oligodendroglia, stomatognathic diseases, 030104 developmental biology, medicine.anatomical_structure, p21-Activated Kinases, Neurology, nervous system, PAK3, Differentiation, Knockout mouse, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Neuroscience, OPC, 030217 neurology & neurosurgery
Abstract

International audience; Oligodendrocyte and myelin deficits have been reported in mental/psychiatric diseases. The p21-activated kinase 3 (PAK3), a serine/threonine kinase, whose activity is stimulated by the binding of active Rac and Cdc42 GTPases is affected in these pathologies. Indeed, many mutations of Pak3 gene have been described in non-syndromic intellectual disability diseases. Pak3 is expressed mainly in the brain where its role has been investigated in neurons but not in glial cells. Here, we showed that PAK3 is highly expressed in oligodendrocyte precursors (OPCs) and its expression decreases in mature oligodendrocytes. In the developing white matter of the Pak3 knockout mice, we found defects of oligodendrocyte differentiation in the corpus callosum and to a lesser extent in the anterior commissure, which were compensated at the adult stage. In vitro experiments in OPC cultures, derived from Pak3 knockout and wild type brains, support a developmental and cell-autonomous role for PAK3 in regulating OPC differentiation into mature oligodendrocytes. Moreover, we did not detect any obvious alterations of the proliferation or migration of Pak3 null OPCs compared to wild type. Overall, our data highlight PAK3 as a new regulator of OPC differentiation.

Published
2017
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3. Silencing of the Charcot-Marie-Tooth associated MTMR2 gene decreases proliferation and enhances cell death in primary cultures of Schwann cells

Author

Anne Baron-Van Evercooren, Bernard Brugg, Corinne Bachelin, Nicole Ravisé, Jocelyn Laporte, Christel Depienne, Merle Ruberg, Alexandre Chojnowski, Eric LeGuern, Neurologie et thérapeutique expérimentale, Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR70-Institut National de la Santé et de la Recherche Médicale (INSERM), Affections de la Myeline et des Canaux Ioniques Musculaires, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Neurobiologie des processus adaptatifs (NPA), Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS), Département d'Astrophysique, de physique des Particules, de physique Nucléaire et de l'Instrumentation Associée (DAPNIA), Commissariat à l'énergie atomique et aux énergies alternatives (CEA), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), This work was supported by the Association Francaise contre les Myopathies (AFM), by Association de Recherche sur les Maladies Génétiques Neurologiques et Psychiatriques (ADRMGNP) and INSERM. A.C., N.R., A. B.-V. and E.L. are members of the 'GIS-Orphan' diseases research network on autosomal recessive forms of CMT. A.C. was supported by AFM., Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR70-Université Pierre et Marie Curie - Paris 6 (UPMC), and Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
Schwann, Myotubularin, "Apoptosis", Proliferation, Apoptosis, Culture Media, Serum-Free, 0302 clinical medicine, RNA interference, Charcot-Marie-Tooth Disease, Cells, Cultured, Myelin Sheath, "Schwann", 0303 health sciences, Charcot–Marie–Tooth, Cell Death, Gene Expression Regulation, Developmental, [SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences, Protein Tyrosine Phosphatases, Non-Receptor, Cell biology, medicine.anatomical_structure, Neurology, Peripheral nervous system, Caspases, RNA Interference, Programmed cell death, "RNAi", Down-Regulation, Biology, lcsh:RC321-571, "Charcot–Marie–Tooth", 03 medical and health sciences, "Proliferation", medicine, Gene silencing, Animals, Gene Silencing, Peripheral Nerves, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Gene, Loss function, 030304 developmental biology, Cell Proliferation, Gene Expression Profiling, ACM, Rats, MTMR2, Animals, Newborn, nervous system, RNAi, Immunology, Schwann Cells, "MTMR2", Protein Tyrosine Phosphatases, 030217 neurology & neurosurgery
Abstract

Loss of function of the myotubularin (MTM)-related protein 2 (MTMR2) in Schwann cells causes Charcot–Marie–Tooth disease type 4B1, a severe demyelinating neuropathy, but the consequences of MTMR2 disruption in Schwann cells are unknown. We established the expression profile of MTMR2 by real-time RT-PCR during rat myelination and showed it to be preferentially expressed at the onset of the myelination period. We developed a model in which MTMR2 loss of function was reproduced in primary cultures of Schwann cells by RNA interference. We found that depletion of MTMR2 in Schwann cells decreased their rate of proliferation. Furthermore, when cultivated in serum-free medium, MTMR2 depletion increased the number of Schwann cells that died by a caspase-dependent process. These results support the hypothesis that loss of MTMR2 in patients, by decreasing Schwann cells proliferation and survival, may impair the first stages of myelination of the peripheral nervous system.

Published
2007
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4. Cultured peripheral neuroglial cells are highly permissive to sheep prion infection

Author

Didier Vilette, Annick Le Dur, Gregory Perrot, Christelle Langevin, Anne Baron-Van Evercooren, Hubert Laude, Corinne Bachelin, Olivier Andreoletti, Fabienne Archer, Nathalie Besnard, Jean-Luc Vilotte, Unité de recherche Virologie et Immunologie Moléculaires (VIM (UR 0892)), Institut National de la Recherche Agronomique (INRA), Affections de la Myeline et des Canaux Ioniques Musculaires, Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Interactions hôtes-agents pathogènes [Toulouse] (IHAP), Institut National de la Recherche Agronomique (INRA)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, and Unité de recherche Génétique Biochimique et Cytogénétique (LGBC)

Subjects
PrPSc Proteins, animal diseases, Immunology, Cell, Central nervous system, Mice, Transgenic, Scrapie, Biology, Microbiology, Virus, Mice, 03 medical and health sciences, 0302 clinical medicine, Antigen, Ganglia, Spinal, Virology, Peripheral Nervous System, medicine, Animals, PrPC Proteins, Cells, Cultured, 030304 developmental biology, Neurons, Infectivity, 0303 health sciences, Sheep, 3. Good health, nervous system diseases, medicine.anatomical_structure, Cell culture, Insect Science, Peripheral nervous system, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, Pathogenesis and Immunity, Female, Schwann Cells, Neuroglia, 030217 neurology & neurosurgery
Abstract

Transmissible spongiform encephalopathies arise as a consequence of infection of the central nervous system (CNS) by prions. Spreading of the infectious agent through the peripheral nervous system (PNS) may represent a crucial step toward CNS neuroinvasion, but the modalities of this process have yet to be clarified. Here we provide further evidence that PNS glial cells are likely targets for infection by prions. Glial cell clones originating from dorsal root ganglia of transgenic mice expressing ovine PrP (tgOv) and simian virus 40 T antigen were found to be readily infectible by sheep scrapie agent. This led us to establish two stable cell lines that exhibited features of Schwann cells. These cells were shown to sustain an efficient and stable replication of sheep prion based on the high level of accumulation of abnormal PrP and infectivity in exposed cultures. We also provide evidence for abnormal PrP deposition in peripheral neuroglial cells from scrapie-infected tgOv mice and sheep. These findings have potential implications in terms of designing new cell systems permissive to prions and of peripheral pathobiology of prion infections.

Published
2004
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