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6 results on '"Da Barroca, Sandra"'

1. Novel UBQLN2 mutations linked to amyotrophic lateral sclerosis and atypical hereditary spastic paraplegia phenotype through defective HSP70-mediated proteolysis

Author

Teyssou, Elisa, Chartier, Laura, Amador, Maria-Del-Mar, Lam, Roselina, Lautrette, Géraldine, Nicol, Marie, Machat, Selma, Da Barroca, Sandra, Moigneu, Carine, Mairey, Mathilde, Larmonier, Thierry, Saker, Safaa, Dussert, Christelle, Forlani, Sylvie, Fontaine, Bertrand, Seilhean, Danielle, Bohl, Delphine, Boillée, Séverine, Meininger, Vincent, Couratier, Philippe, Salachas, François, Stevanin, Giovanni, and Millecamps, Stéphanie

Published
2017
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2. Aggregation of Engineered Human β-Cells Into Pseudoislets: Insulin Secretion and Gene Expression Profile in Normoxic and Hypoxic Milieu

Author

Lecomte, Marie-José, Pechberty, Séverine, Machado, Cécile, Da Barroca, Sandra, Ravassard, Philippe, Scharfmann, Raphaël, Czernichow, Paul, Duvillié, Bertrand, Centre de Recherche des Cordeliers ( CRC ), Université Paris Diderot - Paris 7 ( UPD7 ) -École pratique des hautes études ( EPHE ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute ( ICM ), 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 ) -CHU Pitié-Salpêtrière [APHP], Université Paris Descartes - Faculté de Médecine ( UPD5 Médecine ), Université Paris Descartes - Paris 5 ( UPD5 ), Institut Cochin ( UM3 (UMR 8104 / U1016) ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Centre de Recherche des Cordeliers (CRC), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), 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)-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), Université Paris Descartes - Faculté de Médecine (UPD5 Médecine), Université Paris Descartes - Paris 5 (UPD5), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-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)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 (UPMC)-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)-Centre National de la Recherche Scientifique (CNRS), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), and 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)-CHU Pitié-Salpêtrière [APHP]

Subjects
Pseudoislets (PIs), [ SDV.BC ] Life Sciences [q-bio]/Cellular Biology, Insulin secretion, [ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathology, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, HIF1α, Hypoxia, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, β-Cells
Abstract

International audience; Innovative treatments to cure type 1 diabetes are being actively researched. Among the different strategies, the replacement of β-cells has given promising results. Classically, islets from cadaveric donors are transplanted into diabetic patients, but recently phase I clinical trials that use stem cell-derived β-cells have been started. Such protocols require either an immunosuppressive treatment or the macroencapsulation of the β-cells. They involve cell aggregation and the exposure of the cells to hypoxia. Using an engineered human β-cell, we have addressed these two problems: a novel human β-cell line called EndoC-βH3 was cultured as single cells or aggregated clusters. EndoC-βH3 cells were also cultured at normal atmospheric oxygen tension (pO2 = 21%) or hypoxia (pO2 = 3%) in the presence or absence of modulators of the hypoxia-inducible factor 1α (HIF1α) pathway. Cell aggregation improved glucose-stimulated insulin secretion, demonstrating the benefit of cell–cell contacts. Low oxygen tension decreased β-cell viability and their sensitivity to glucose, but did not alter insulin production nor the insulin secretion capacity of the remaining cells. To investigate the role of HIF1α, we first used a HIF stabilizer at pO2 = 21%. This led to a mild decrease in cell viability, impaired glucose sensitivity, and altered insulin secretion. Finally, we used a HIF inhibitor on EndoC-βH3 pseudoislets exposed to hypoxia. Such treatment considerably decreased cell viability. In conclusion, aggregation of the EndoC-βH3 cells seems to be important to improve their function. A fraction of the EndoC-βH3 cells are resistant to hypoxia, depending on the level of activity of HIF1α. Thus, these cells represent a good human cell model for future investigations on islet cell transplantation analysis.

Published
2016

4. Contribution of ATXN2 intermediary polyQ expansions in a spectrum of neurodegenerative disorders.

Author

Lattante, Serena, Millecamps, Stéphanie, Stevanin, Giovanni, Rivaud-Péchoux, Sophie, Moigneu, Carine, Camuzat, Agnès, Da Barroca, Sandra, Mundwiller, Emeline, Couarch, Philippe, Salachas, François, Hannequin, Didier, Meininger, Vincent, Pasquier, Florence, Seilhean, Danielle, Couratier, Philippe, Danel-Brunaud, Véronique, Bonnet, Anne-Marie, Tranchant, Christine, LeGuern, Eric, and Brice, Alexis

Published
2014
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5. Contribution of ATXN2intermediary polyQ expansions in a spectrum of neurodegenerative disorders

Author

Lattante, Serena, Millecamps, Stéphanie, Stevanin, Giovanni, Rivaud-Péchoux, Sophie, Moigneu, Carine, Camuzat, Agnès, Da Barroca, Sandra, Mundwiller, Emeline, Couarch, Philippe, Salachas, François, Hannequin, Didier, Meininger, Vincent, Pasquier, Florence, Seilhean, Danielle, Couratier, Philippe, Danel-Brunaud, Véronique, Bonnet, Anne-Marie, Tranchant, Christine, LeGuern, Eric, Brice, Alexis, Le Ber, Isabelle, and Kabashi, Edor

Abstract

The aim of this study was to establish the frequency of ATXN2polyglutamine (polyQ) expansion in large cohorts of patients with amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and progressive supranuclear palsy (PSP), and to evaluate whether ATXN2could act as a modifier gene in patients carrying the C9orf72expansion.

Published
2014
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6. Questioning on the role of D amino acid oxidase in familial amyotrophic lateral sclerosis.

Author

Millecamps S, Da Barroca S, Cazeneuve C, Salachas F, Pradat PF, Danel-Brunaud V, Vandenberghe N, Lacomblez L, Le Forestier N, Bruneteau G, Camu W, Brice A, Meininger V, and LeGuern E

Subjects
Amino Acid Sequence, Amino Acid Substitution, Base Sequence, Conserved Sequence, DNA genetics, DNA Mutational Analysis, Exons, Female, Heterozygote, Humans, Male, Molecular Sequence Data, Mutation, Missense, Pedigree, Polymorphism, Single Nucleotide, Sequence Homology, Amino Acid, Species Specificity, Amyotrophic Lateral Sclerosis enzymology, Amyotrophic Lateral Sclerosis genetics, D-Amino-Acid Oxidase genetics, Genetic Variation
Published
2010
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