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2. Microglial glucocorticoid receptors play a pivotal role in regulating dopaminergic neurodegeneration in parkinsonism

Author

Ros-Bernal, Francisco, Hunot, Stéphane, Herrero, Maria Trinidad, Parnadeau, Sebastien, Corvol, Jean-Christophe, Lu, Lixia, Alvarez-Fischer, Daniel, Carrillo-de Sauvage, María Angeles, Saurini, Françoise, Coussieu, Christiane, Kinugawa, Kiyoka, Prigent, Annick, Höglinger, Günter, Hamon, Michel, Tronche, François, Hirsch, Etienne C., Vyas, Sheela, and Gage, Fred H.

Published
2011

5. TLR9 activation via microglial glucocorticoid receptors contributes to degeneration of midbrain dopamine neurons

Author

Maatouk, Layal, Compagnion, Anne-Claire, Sauvage, Maria-Angeles Carrillo-De, Bemelmans, Alexis-Pierre, Leclere-Turbant, Sabrina, Cirotteau, Vincent, Tohmé, Mira, Beke, Allen, Trichet, Michael, Bazin, Virginie, Trawick, Bobby, Ransohoff, Richard, Tronche, Francois, Manoury, Bénédicte, Vyas, Sheela, Neurosciences Paris Seine (NPS), Sorbonne Université (SU)-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)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), 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), Service MIRCEN (MIRCEN), 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)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Institut de neurosciences translationnelles de Paris (NeurATRIS - IHU-A-ICM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Institut Necker Enfants-Malades (INEM - UM 111 (UMR 8253 / U1151)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Microscopie Electronique [IBPS] (IBPS-ME), 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), Mallinckrodt Pharmaceuticals, Third Rock Ventures, ANR-13-BSV1-0013,ParkSTRIM,Rôle des altérations du système immunitaire et des fonctions neuronales induites par le stress dans les mécanismes physiopathologiques de la maladie de Parkinson.(2013), Neuroscience Paris Seine (NPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), CHU Pitié-Salpêtrière [APHP], 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), Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie François JACOB (JACOB), 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)-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), Savelli, Bruno, and Blanc 2013 - Rôle des altérations du système immunitaire et des fonctions neuronales induites par le stress dans les mécanismes physiopathologiques de la maladie de Parkinson. - - ParkSTRIM2013 - ANR-13-BSV1-0013 - Blanc 2013 - VALID

Subjects
[SDV] Life Sciences [q-bio], [SDV.IB] Life Sciences [q-bio]/Bioengineering, [SDV]Life Sciences [q-bio], Science, lcsh:Q, [SDV.IB]Life Sciences [q-bio]/Bioengineering, lcsh:Science, ComputingMilieux_MISCELLANEOUS, nervous system diseases
Abstract

Inflammation is a component of Parkinson’s disease. Here the authors show that activation of Toll-like receptor 9 controlled by microglial glucocorticoid receptor signaling, contributes to dopamine neuron loss in a model of Parkinson’s disease.

Published
2018

7. Glucocorticoid receptor in astrocytes regulates midbrain dopamine neurodegeneration through connexin hemichannel activity

Author

Maatouk, Layal, Yi, Chenju, Carrillo-de Sauvage, Maria-Angeles, Compagnion, Anne-Claire, Hunot, Stéphane, Ezan, Pascal, Hirsch, Etienne, Koulakoff, Annette, Pfrieger, Frank, Tronche, Francois, Leybaert, Luc, Giaume, Christian, Vyas, Sheela, Neurosciences Paris Seine (NPS), Sorbonne Université (SU)-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)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Centre interdisciplinaire de recherche en biologie (CIRB), Labex MemoLife, École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire des Maladies Neurodégénératives - UMR 9199 (LMN), Centre National de la Recherche Scientifique (CNRS)-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), 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], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Institut des Neurosciences Cellulaires et Intégratives (INCI), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Universiteit Gent = Ghent University [Belgium] (UGENT), Neuroscience Paris Seine (NPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Collège de France (CdF)-Institut National de la Santé et de la Recherche Médicale (INSERM)-PSL Research University (PSL)-Centre National de la Recherche Scientifique (CNRS), Université Paris-Sud - Paris 11 (UP11)-Service MIRCEN (MIRCEN), 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 de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [APHP]-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Ghent University [Belgium] (UGENT), École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS-PSL), Service MIRCEN (MIRCEN), 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), 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 Universiteit Gent = Ghent University (UGENT)

Subjects
MICROGLIA, ACTIVATION, PARKINSONS-DISEASE, ALPHA-SYNUCLEIN, INFLAMMATION, CX43 HEMICHANNELS, [SDV]Life Sciences [q-bio], Medicine and Health Sciences, Biology and Life Sciences, MOUSE MODEL, COMMUNICATION, GENE, MECHANISMS
Abstract

International audience; The precise contribution of astrocytes in neuroinflammatory process occurring in Parkinson’s disease (PD) is not well characterized. In this study, using GRCx30CreERT2 mice that are conditionally inactivated for glucocorticoid receptor (GR) in astrocytes, we have examined the actions of astrocytic GR during dopamine neuron (DN) degeneration triggered by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The results show significantly augmented DN loss in GRCx30CreERT2 mutant mice in substantia nigra (SN) compared to controls. Hypertrophy of microglia but not of astrocytes was greatly enhanced in SN of these astrocytic GR mutants intoxicated with MPTP, indicating heightened microglial reactivity compared to similarly-treated control mice. In the SN of GR astrocyte mutants, specific inflammation-associated transcripts ICAM-1, TNF-α and Il-1β as well as TNF-α protein levels were significantly elevated after MPTP neurotoxicity compared to controls. Interestingly, this paralleled increased connexin hemichannel activity and elevated intracellular calcium levels in astrocytes examined in acute midbrain slices from control and mutant mice treated with MPP+ . The increased connexin-43 hemichannel activity was found in vivo in MPTP-intoxicated mice. Importantly, treatment of MPTP-injected GRCx30CreERT2 mutant mice with TAT-Gap19 peptide, a specific connexin-43 hemichannel blocker, reverted both DN loss and microglial activation; in wild-type mice there was partial but significant survival effect. In the SN of post-mortem PD patients, a significant decrease in the number of astrocytes expressing nuclear GR was observed, suggesting the participation of astrocytic GR deregulation of inflammatory process in PD. Overall, these data provide mechanistic insights into GR-modulated processes in vivo, specifically in astrocytes, that contribute to a pro-inflammatory state and dopamine neurodegeneration in PD pathology.

Published
2018

8. Author Correction: TLR9 activation via microglial glucocorticoid receptors contributes to degeneration of midbrain dopamine neurons

Author

Maatouk, Layal, primary, Compagnion, Anne-Claire, additional, Sauvage, Maria-Angeles Carrillo-de, additional, Bemelmans, Alexis-Pierre, additional, Leclere-Turbant, Sabrina, additional, Cirotteau, Vincent, additional, Tohme, Mira, additional, Beke, Allen, additional, Trichet, Michaël, additional, Bazin, Virginie, additional, Trawick, Bobby N., additional, Ransohoff, Richard M., additional, Tronche, François, additional, Manoury, Bénédicte, additional, and Vyas, Sheela, additional

Published
2018
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9. Caspase-3: A vulnerability factor and final effector in apoptotic death of dopaminergic neurons in Parkinson's disease

Author

Hartmann, Andreas, Hunot, Stephane, Michel, Patrick P., Muriel, Marie-Paule, Vyas, Sheela, Faucheux, Baptiste A., Mouatt-Prigent, Annick, Turmel, Helene, Srinivasan, Anu, Ruberg, Merle, Evan, Gerard I., Agid, Yves, and Hirsh, Etienne C.

Subjects
Cell death -- Analysis, Parkinson's disease -- Research, Dopamine -- Agonists, Brain research -- Research, Science and technology
Abstract

Caspase-3 is an effector of apoptosis in experimental models of Parkinson's disease (PD). However, its potential role in the human pathology remains to be demonstrated. Using caspase-3 immuno-histochemistry on the postmortem human brain, we observed a positive correlation between the degree of neuronal loss in dopaminergic (DA) cell groups affected in the mesencephalon of PD patients and the percentage of caspase-3-positive neurons in these cell groups in control subjects and a significant decrease of caspase-3-positive pigmented neurons in the substantia nigra pars compacta of PD patients compared with controls that also could be observed in an animal model of PD. This suggests that neurons expressing caspase-3 are more sensitive to the pathological process than those that do not express the protein. In addition, using an antibody raised against activated caspase-3, the percentage of active caspase-3-positive neurons among DA neurons was significantly higher in PD patients than in controls. Finally, electron microscopy analysis in the human brain and in vitro data suggest that caspase-3 activation precedes and is not a consequence of apoptotic cell death in PD.

Published
2000

16. Macrophage-Derived Tumor Necrosis Factor α, an Early Developmental Signal for Motoneuron Death.

Author

Sedel, Frédéric, Béchade, Catherine, Vyas, Sheela, and Triller, Antoine

Subjects
TUMOR necrosis factors, MOTOR neurons, CELL death, MACROPHAGES, APOPTOSIS, SOMITE
Abstract

Mechanisms inducing neuronal death at defined times during embryogenesis remain enigmatic. We show in explants that a developmental switch occurs between embryonic day 12 (El2) and El3 in rats that is 72- 48 hr before programmed cell death. Half the motoneurons isolated from peripheral tissues at E12 escape programmed cell death, whereas 90% of motoneurons isolated at El3 enter a death program. The surrounding somite commits El2 motoneurons to death. This effect requires macrophage cells, is mimicked by tumor necrosis factor α (TNFα), and is inhibited by anti-TNFα antibodies. In vivo, TNFα is detected within somite macrophages, and TNF receptor 1 (TNFR 1) is detected within motoneurons precisely between E 12 and E 13. Although motoneuron cell death occurs normally in TNFα-/- mice, this process is significantly reduced in explants from TNFα-/- and TNFR1-/- mice. Thus, embryonic motoneurons acquire the competence to die, before the onset of programmed cell death, from extrinsic signals such as macrophage-derived TNFα. [ABSTRACT FROM AUTHOR]

Published
2004
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17. Macrophage-derived tumor necrosis factor alpha, an early developmental signal for motoneuron death.

Author

Sedel F, Béchade C, Vyas S, and Triller A

Subjects
Animals, Antigens, CD biosynthesis, Apoptosis genetics, Gene Expression Regulation physiology, Mesoderm metabolism, Motor Neurons cytology, RNA, Messenger metabolism, Rats, Rats, Sprague-Dawley, Receptors, Tumor Necrosis Factor biosynthesis, Receptors, Tumor Necrosis Factor, Type I, Somites cytology, Somites physiology, Tumor Necrosis Factor-alpha genetics, Apoptosis physiology, Gene Expression Regulation, Developmental physiology, Macrophages metabolism, Motor Neurons metabolism, Tumor Necrosis Factor-alpha metabolism
Abstract

Mechanisms inducing neuronal death at defined times during embryogenesis remain enigmatic. We show in explants that a developmental switch occurs between embryonic day 12 (E12) and E13 in rats that is 72-48 hr before programmed cell death. Half the motoneurons isolated from peripheral tissues at E12 escape programmed cell death, whereas 90% of motoneurons isolated at E13 enter a death program. The surrounding somite commits E12 motoneurons to death. This effect requires macrophage cells, is mimicked by tumor necrosis factor alpha (TNFalpha), and is inhibited by anti-TNFalpha antibodies. In vivo, TNFalpha is detected within somite macrophages, and TNF receptor 1 (TNFR1) is detected within motoneurons precisely between E12 and E13. Although motoneuron cell death occurs normally in TNFalpha-/- mice, this process is significantly reduced in explants from TNFalpha-/- and TNFR1-/- mice. Thus, embryonic motoneurons acquire the competence to die, before the onset of programmed cell death, from extrinsic signals such as macrophage-derived TNFalpha

Published
2004
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