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3. Co-exposure to benzo[a]pyrene and ethanol induces a pathological progression of liver steatosis in vitro and in vivo

Author

Bucher, Simon, Tête, Arnaud, Podechard, Normand, Liamin, Marie, Le Guillou, Dounia, Chevanne, Martine, Coulouarn, Cédric, IMRAN, Muhammad, Gallais, Isabelle, Fernier, Morgane, Hamdaoui, Quentin, Robin, Marie-Anne, Sergent, Odile, Fromenty, Bernard, Lagadic-Gossmann, Dominique, Nutrition, Métabolismes et Cancer (NuMeCan), Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), École des Hautes Études en Santé Publique [EHESP] (EHESP), Region Bretagne (ARED), Agence Nationale de la Recherche (ANR), ANR (STEATOX project) [ANR-13-CESA-0009], Institut National de la Recherche Agronomique (INRA)-Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), ANR-13-CESA-0009,STEATOX,Impact des agents chimiques environnementaux sur les mécanismes de progression pathologique de la stéatose hépatique(2013), Jonchère, Laurent, and Contaminants et Environnements : Santé, Adaptabilité, Comportements et Usages - Impact des agents chimiques environnementaux sur les mécanismes de progression pathologique de la stéatose hépatique - - STEATOX2013 - ANR-13-CESA-0009 - CESA - VALID

Subjects
toxicant-associated steatohepatitis, hepatocellular-carcinoma, [SDV]Life Sciences [q-bio], drug-metabolism, lcsh:Medicine, chronic exposure, Article, Cell Line, primary rat hepatocytes, Benzo(a)pyrene, Animals, Humans, oxidative stress, cytochrome-p450 expression, lcsh:Science, Zebrafish, Inflammation, Ethanol, hepatic steatosis, lcsh:R, Lipid Metabolism, Rats, Fatty Liver, [SDV] Life Sciences [q-bio], heparg cells, Disease Models, Animal, Liver, Larva, Disease Progression, Environmental Pollutants, lcsh:Q, disrupting chemicals, Biomarkers
Abstract

International audience; Hepatic steatosis (i.e. lipid accumulation) and steatohepatitis have been related to diverse etiologic factors, including alcohol, obesity, environmental pollutants. However, no study has so far analyzed how these different factors might interplay regarding the progression of liver diseases. The impact of the co-exposure to the environmental carcinogen benzo[a]pyrene (B[a]P) and the lifestyle-related hepatotoxicant ethanol, was thus tested on in vitro models of steatosis (human HepaRG cell line; hybrid human/rat WIF-B9 cell line), and on an in vivo model (obese zebrafish larvae). Steatosis was induced prior to chronic treatments (14, 5 or 7 days for HepaRG, WIF-B9 or zebrafish, respectively). Toxicity and inflammation were analyzed in all models; the impact of steatosis and ethanol towards B[a]P metabolism was studied in HepaRG cells. Cytotoxicity and expression of inflammation markers upon co-exposure were increased in all steatotic models, compared to non steatotic counterparts. A change of B[a]P metabolism with a decrease in detoxification was detected in HepaRG cells under these conditions. A prior steatosis therefore enhanced the toxicity of B[a]P/ethanol co-exposure in vitro and in vivo; such a co-exposure might favor the appearance of a steatohepatitis-like state, with the development of inflammation. These deleterious effects could be partly explained by B[a]P metabolism alterations.

Published
2018
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4. Zebrafish larva as a reliable model for in vivo assessment of membrane remodeling involvement in the hepatotoxicity of chemical agents

Author

Podechard, Normand, Chevanne, Martine, Fernier, Morgane, Tête, Arnaud, Collin, Aurore, Cassio, Doris, Kah, Olivier, Lagadic-Gossmann, Dominique, Sergent, Odile, Institut de recherche en santé, environnement et travail (Irset), Université d'Angers (UA)-Université de Rennes (UR)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Signalisation calcique et interactions cellulaires dans le foie, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), Supported by the Institut de Recherches scientifiques sur les Boissons (IREB) (contract numbers 2011/28, 2012/27, 2013/29), by the Agence Nationale de la Recherche (ANR) (STEATOX project, contract number ANR-13-CESA-0009) and also by European Union (FEDER), the Region Bretagne, the Conseil Général d'Ille-et-Vilaine, Rennes Métropole and the French Ministry of High Education and Research (MESR) for the financial support of the project Membratox (Contract number 32508, 350 keuros) and the project 'Modernisation des équipements Rennes 2010–2013: Développement du plateau Membrane et Stress'(70 keuros). This study was also supported by the Structure Fédérative de Recherche en Biologie et Santé de Rennes (BIOSIT). Aurore Collin was a recipient of a fellowship from the Ligue Nationale contre le Cancer., ANR-13-CESA-0009,STEATOX,Impact des agents chimiques environnementaux sur les mécanismes de progression pathologique de la stéatose hépatique(2013), Chard-Hutchinson, Xavier, Contaminants et Environnements : Santé, Adaptabilité, Comportements et Usages - Impact des agents chimiques environnementaux sur les mécanismes de progression pathologique de la stéatose hépatique - - STEATOX2013 - ANR-13-CESA-0009 - CESA - VALID, Université d'Angers (UA)-Université de Rennes 1 (UR1), and Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )

Subjects
hepatotoxicity, Cell Survival, Membrane Fluidity, Hybrid Cells, Models, Biological, Cell Line, Membrane Microdomains, Animals, Humans, [SDV.EE.SANT] Life Sciences [q-bio]/Ecology, environment/Health, Zebrafish, Pravastatin, [SDV.EE.SANT]Life Sciences [q-bio]/Ecology, environment/Health, Ethanol, Ursodeoxycholic Acid, in vivo model, Rats, [SDV.TOX] Life Sciences [q-bio]/Toxicology, Oxidative Stress, chemical agents, Liver, Microscopy, Fluorescence, Larva, [SDV.TOX]Life Sciences [q-bio]/Toxicology, zebrafish larva, membrane remodeling, Chemical and Drug Induced Liver Injury
Abstract

The easy-to-use in vivo model, zebrafish larva, is being increasingly used to screen chemical-induced hepatotoxicity, with a good predictivity for various mechanisms of liver injury. However, nothing is known about its applicability in exploring the mechanism called membrane remodeling, depicted as changes in membrane fluidity or lipid raft properties. The aim of this study was, therefore, to substantiate the zebrafish larva as a suitable in vivo model in this context. Ethanol was chosen as a prototype toxicant because it is largely described, both in hepatocyte cultures and in rodents, as capable of inducing a membrane remodeling leading to hepatocyte death and liver injury. The zebrafish larva model was demonstrated to be fully relevant as membrane remodeling was maintained even after a 1-week exposure without any adaptation as usually reported in rodents and hepatocyte cultures. It was also proven to exhibit a high sensitivity as it discriminated various levels of cytotoxicity depending on the extent of changes in membrane remodeling. In this context, its sensitivity appeared higher than that of WIF-B9 hepatic cells, which is suited for analyzing this kind of hepatotoxicity. Finally, the protection afforded by a membrane stabilizer, ursodeoxycholic acid (UDCA), or by a lipid raft disrupter, pravastatin, definitely validated zebrafish larva as a reliable model to quickly assess membrane remodeling involvement in chemical-induced hepatotoxicity. In conclusion, this model, compatible with a high throughput screening, might be adapted to seek hepatotoxicants via membrane remodeling, and also drugs targeting membrane features to propose new preventive or therapeutic strategies in chemical-induced liver diseases. Copyright © 2016 John WileySons, Ltd.

Published
2017
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6. Role for the ATPase inhibitory factor 1 in the environmental carcinogen-induced Warburg phenotype

Author

Hardonnière, Kévin, primary, Fernier, Morgane, additional, Gallais, Isabelle, additional, Mograbi, Baharia, additional, Podechard, Normand, additional, Le Ferrec, Eric, additional, Grova, Nathalie, additional, Appenzeller, Brice, additional, Burel, Agnès, additional, Chevanne, Martine, additional, Sergent, Odile, additional, Huc, Laurence, additional, Bortoli, Sylvie, additional, and Lagadic-Gossmann, Dominique, additional

Published
2017
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8. The environmental carcinogen benzo[a]pyrene induces a Warburg-like metabolic reprogramming dependent on NHE1 and associated with cell survival

Author

Hardonnière, Kévin, primary, Saunier, Elise, additional, Lemarié, Anthony, additional, Fernier, Morgane, additional, Gallais, Isabelle, additional, Héliès-Toussaint, Cécile, additional, Mograbi, Baharia, additional, Antonio, Samantha, additional, Bénit, Paule, additional, Rustin, Pierre, additional, Janin, Maxime, additional, Habarou, Florence, additional, Ottolenghi, Chris, additional, Lavault, Marie-Thérèse, additional, Benelli, Chantal, additional, Sergent, Odile, additional, Huc, Laurence, additional, Bortoli, Sylvie, additional, and Lagadic-Gossmann, Dominique, additional

Published
2016
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9. Co-exposure to benzo[a]pyrene and ethanol induces a pathological progression of liver steatosis in vitro and in vivo.

Author

Bucher S, Tête A, Podechard N, Liamin M, Le Guillou D, Chevanne M, Coulouarn C, Imran M, Gallais I, Fernier M, Hamdaoui Q, Robin MA, Sergent O, Fromenty B, and Lagadic-Gossmann D

Subjects
Animals, Biomarkers metabolism, Cell Line, Disease Models, Animal, Disease Progression, Environmental Pollutants adverse effects, Fatty Liver metabolism, Humans, Inflammation metabolism, Inflammation pathology, Larva metabolism, Lipid Metabolism drug effects, Liver metabolism, Rats, Zebrafish, Benzo(a)pyrene adverse effects, Ethanol adverse effects, Fatty Liver pathology, Liver pathology
Abstract

Hepatic steatosis (i.e. lipid accumulation) and steatohepatitis have been related to diverse etiologic factors, including alcohol, obesity, environmental pollutants. However, no study has so far analyzed how these different factors might interplay regarding the progression of liver diseases. The impact of the co-exposure to the environmental carcinogen benzo[a]pyrene (B[a]P) and the lifestyle-related hepatotoxicant ethanol, was thus tested on in vitro models of steatosis (human HepaRG cell line; hybrid human/rat WIF-B9 cell line), and on an in vivo model (obese zebrafish larvae). Steatosis was induced prior to chronic treatments (14, 5 or 7 days for HepaRG, WIF-B9 or zebrafish, respectively). Toxicity and inflammation were analyzed in all models; the impact of steatosis and ethanol towards B[a]P metabolism was studied in HepaRG cells. Cytotoxicity and expression of inflammation markers upon co-exposure were increased in all steatotic models, compared to non steatotic counterparts. A change of B[a]P metabolism with a decrease in detoxification was detected in HepaRG cells under these conditions. A prior steatosis therefore enhanced the toxicity of B[a]P/ethanol co-exposure in vitro and in vivo; such a co-exposure might favor the appearance of a steatohepatitis-like state, with the development of inflammation. These deleterious effects could be partly explained by B[a]P metabolism alterations.

Published
2018
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10. Zebrafish larva as a reliable model for in vivo assessment of membrane remodeling involvement in the hepatotoxicity of chemical agents.

Author

Podechard N, Chevanne M, Fernier M, Tête A, Collin A, Cassio D, Kah O, Lagadic-Gossmann D, and Sergent O

Subjects
Animals, Cell Line, Cell Survival drug effects, Chemical and Drug Induced Liver Injury etiology, Chemical and Drug Induced Liver Injury pathology, Chemical and Drug Induced Liver Injury prevention & control, Ethanol toxicity, Humans, Hybrid Cells, Larva metabolism, Liver metabolism, Liver pathology, Membrane Microdomains pathology, Microscopy, Fluorescence, Oxidative Stress drug effects, Pravastatin pharmacology, Rats, Ursodeoxycholic Acid pharmacology, Larva drug effects, Liver drug effects, Membrane Fluidity drug effects, Membrane Microdomains drug effects, Models, Biological, Zebrafish
Abstract

The easy-to-use in vivo model, zebrafish larva, is being increasingly used to screen chemical-induced hepatotoxicity, with a good predictivity for various mechanisms of liver injury. However, nothing is known about its applicability in exploring the mechanism called membrane remodeling, depicted as changes in membrane fluidity or lipid raft properties. The aim of this study was, therefore, to substantiate the zebrafish larva as a suitable in vivo model in this context. Ethanol was chosen as a prototype toxicant because it is largely described, both in hepatocyte cultures and in rodents, as capable of inducing a membrane remodeling leading to hepatocyte death and liver injury. The zebrafish larva model was demonstrated to be fully relevant as membrane remodeling was maintained even after a 1-week exposure without any adaptation as usually reported in rodents and hepatocyte cultures. It was also proven to exhibit a high sensitivity as it discriminated various levels of cytotoxicity depending on the extent of changes in membrane remodeling. In this context, its sensitivity appeared higher than that of WIF-B9 hepatic cells, which is suited for analyzing this kind of hepatotoxicity. Finally, the protection afforded by a membrane stabilizer, ursodeoxycholic acid (UDCA), or by a lipid raft disrupter, pravastatin, definitely validated zebrafish larva as a reliable model to quickly assess membrane remodeling involvement in chemical-induced hepatotoxicity. In conclusion, this model, compatible with a high throughput screening, might be adapted to seek hepatotoxicants via membrane remodeling, and also drugs targeting membrane features to propose new preventive or therapeutic strategies in chemical-induced liver diseases. Copyright © 2016 John Wiley & Sons, Ltd., (Copyright © 2016 John Wiley & Sons, Ltd.)

Published
2017
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