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Your search keyword '"CAMPOS, S."' showing total 27 results
Start Over Author "CAMPOS, S." Journal journal of hepatology
27 results on '"CAMPOS, S."'

1. Comprehensive analysis and insights gained from long-term experience of the Spanish DILI Registry

Author

Stephens, Camilla, primary, Robles-Diaz, Mercedes, additional, Medina-Caliz, Inmaculada, additional, Garcia-Cortes, Miren, additional, Ortega-Alonso, Aida, additional, Sanabria-Cabrera, Judith, additional, Gonzalez-Jimenez, Andres, additional, Alvarez-Alvarez, Ismael, additional, Slim, Mahmoud, additional, Jimenez-Perez, Miguel, additional, Gonzalez-Grande, Rocio, additional, Fernández, M. Carmen, additional, Casado, Marta, additional, Soriano, German, additional, Román, Eva, additional, Hallal, Hacibe, additional, Romero-Gomez, Manuel, additional, Castiella, Agustin, additional, Conde, Isabel, additional, Prieto, Martin, additional, Moreno-Planas, Jose Maria, additional, Giraldez, Alvaro, additional, Moreno-Sanfiel, J. Miguel, additional, Kaplowitz, Neil, additional, Lucena, M. Isabel, additional, Andrade, Raúl J., additional, Andrade, R.J., additional, Lucena, M.I., additional, Stephens, C., additional, Cortés, M. García, additional, Robles-Díaz, M., additional, Ortega-Alonso, A., additional, Pinazo, J., additional, Muñoz, B. García, additional, Alcántara, R., additional, Hernández, A., additional, Escaño, M.D. García, additional, del Campo, E., additional, Medina-Cáliz, I., additional, Sanabria-Cabrera, J., additional, González-Jiménez, A., additional, Sanjuán-Jiménez, R., additional, Cueto, A., additional, Álvarez-Álvarez, I., additional, Bonilla, E., additional, Di Zeo, D., additional, Niu, H., additional, Villanueva, M., additional, Papineau, A., additional, Pérez, M. Jiménez, additional, Grande, R. González, additional, Ortega, S. López, additional, Santaella, I., additional, Ocaña, A., additional, Palomino, P., additional, Fernández, M.C., additional, Peláez, G., additional, Porcel, A., additional, Casado, M., additional, Sánchez, M. González, additional, Romero-Gómez, M., additional, Millán-Domínguez, R., additional, Fombuena, B., additional, Gallego, R., additional, Ampuero, J., additional, Campo, J.A. del, additional, Calle-Sanz, R., additional, Rojas, L., additional, Rojas, A., additional, Gómez, A. Gil, additional, Vilar, E., additional, Soriano, G., additional, Guarner, C., additional, Román, E.M., additional, Manuitt, M.A. Quijada, additional, Arbos, R.M. Antonijoan, additional, Delgado, J. Sánchez, additional, Gómez, M. Vergara, additional, Hallal, H., additional, Oltra, E. García, additional, Arcos, J.C. Titos, additional, Martínez, A. Pérez, additional, Cobarro, C. Sánchez, additional, Caparrós, J.M. Egea, additional, Castiella, A., additional, Zapata, E., additional, Arenas, J., additional, García, A. Gómez, additional, Esandi, F.J., additional, Blanco, S., additional, Odriozola, P. Martínez, additional, Crespo, J., additional, Iruzubieta, P., additional, Cabezas, J., additional, Gallego, A. Giráldez, additional, Rodríguez Seguel, E. del P., additional, Cuaresma, M., additional, Gallego, J. González, additional, Jorquera, F., additional, Campos, S. Sánchez, additional, Otazua, P., additional, de Juan Gómez, A., additional, Salmerón, J., additional, Gila, A., additional, Quiles, R., additional, González, J.M., additional, Lorenzo, S., additional, Prieto, M., additional, Amiel, I. Conde, additional, Berenguer, M., additional, García-Eliz, M., additional, Primo, J., additional, Molés, J.R., additional, Garayoa, A., additional, Carrascosa, M., additional, Domínguez, E. Gómez, additional, Cuevas, L., additional, Farré, M., additional, Montané, E., additional, Barriocanal, A.M., additional, Arellano, A.L., additional, Sanz, Y., additional, Morillas, R.M., additional, Sala, M., additional, Ridaura, H. Masnou, additional, Bruguera, M., additional, Gines, P., additional, Lens, S., additional, García, J.C., additional, Mariño, Z., additional, Guerra, M. Hernández, additional, Sanfiel, J.M. Moreno, additional, Fernández del Campo, C. Boada, additional, Tejedor, M., additional, Ferrer, R. González, additional, Fernández, C., additional, Gil, M. Fernández, additional, Montero, J.L., additional, Mata, M. de la, additional, Olmo, J. Fuentes, additional, Bonilla, E.M. Fernández, additional, Moreno, J.M., additional, Martínez-Rodenas, P., additional, Garrido, M., additional, Oliva, C., additional, Rendón, P., additional, Samaniego, J. García, additional, Madejón, A., additional, Calleja, J.L., additional, Porras, J.L. Martínez, additional, Cabriada, J.L., additional, Pérez-Moreno, J.M., additional, and Lara, C., additional

Published
2021
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2. Akkermansia spp. mediates protection from obesity-associated NAFLD development in germ free mice following intestinal microbiota transplantation from high fat diet and quercetin treated donors

Author

Porras, D., primary, Nistal, E., additional, Martínez-Flórez, S., additional, Olcoz-Goni, J.L., additional, Jover, R., additional, Jorquera, F., additional, González-Gállego, J., additional, Garcia-Mediavilla, M.-V., additional, and Sánchez-Campos, S., additional

Published
2018
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6. Protective effect of quercetin treatment on HFD-induced intestinal dysbiosis and barrier dysfunction in an in vivo model of non-alcoholic fatty liver disease

Author

Porras, D., primary, García-Mediavilla, M.V., additional, Nistal, E., additional, Martínez-Florez, S., additional, Pisonero-Vaquero, S., additional, Jorquera, F., additional, Olcoz, J.L., additional, Jover, R., additional, González-Gallego, J., additional, and Sánchez-Campos, S., additional

Published
2017
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11. P0973 : Quercetin ameliorates MCD-induced non-alcoholic fatty liver disease in mice by modulating inflammatory, oxidative/nitrosative stress and lipid metabolism-related gene deregulation via the PI3K/AKT pathway

Author

Pisonero-Vaquero, S., primary, Martínez-Ferreras, Á., additional, García-Mediavilla, M.V., additional, Martínez-Flórez, S., additional, Fernández, A., additional, Benet, M., additional, Olcoz, J.L., additional, Jover, R., additional, González-Gallego, J., additional, and Sánchez-Campos, S., additional

Published
2015
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18. 356 ENHANCED EXPRESSION OF LIVER X RECEPTOR AND ITS LIPOGENIC AND INFLAMMATORY TARGETS IN NONALCOHOLIC FATTY LIVER DISEASE AND CHRONIC HEPATITIS C

Author

Lima, E., primary, García-Mediavilla, M.V., additional, Miquilena-Colina, M.E., additional, Vargas-Castrillón, J., additional, Lozano-Rodríguez, T., additional, Fernández-Bermejo, M., additional, Olcoz, J.L., additional, González-Gallego, J., additional, García-Monzón, C., additional, and Sánchez-Campos, S., additional

Published
2010
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25. Hepatocyte vitamin D receptor regulates lipid metabolism and mediates experimental diet-induced steatosis.

Author

Bozic M, Guzmán C, Benet M, Sánchez-Campos S, García-Monzón C, Gari E, Gatius S, Valdivielso JM, and Jover R

Subjects
Animals, Diet, High-Fat, Disease Models, Animal, Hepatocytes, Humans, Liver, Mice, Mice, Inbred C57BL, Non-alcoholic Fatty Liver Disease, Receptors, Calcitriol, Lipid Metabolism
Abstract

Background & Aims: The pathogenesis and progression of non-alcoholic fatty liver disease (NAFLD) is still incompletely understood. Several nuclear receptors play a role in liver lipid metabolism and can promote hepatosteatosis, but the possible role of vitamin D receptor (VDR) in NAFLD has not been investigated., Methods: The expression of liver VDR was investigated in apolipoprotein E knockout (apoE(-/-)) mice on a high fat diet, in wild-type mice on methionine and choline deficient diet and in NAFLD patients with hepatosteatosis and non-alcoholic steatohepatitis. The relevance of VDR was assessed in apoE(-/-) mice by deletion of VDR or paricalcitol treatment and in human HepG2 cells by VDR transfection or silencing. The role of VDR in fibrosis was also determined in VDR knockout mice (VDR(-/-)) treated with thioacetamide., Results: Expression of liver VDR was markedly induced in two mouse models of NAFLD, as well as in patients with hepatosteatosis, but decreased in non-alcoholic steatohepatitis. VDR deletion in high fat diet-fed apoE(-/-) mice protected against fatty liver, dyslipidemia and insulin resistance, and caused a decrease in taurine-conjugated bile acids, but did not influence fibrosis by thioacetamide. apoE(-/-)VDR(-/-) mouse livers showed decreased gene expression of CD36, DGAT2, C/EBPα and FGF21, and increased expression of PNPLA2, LIPIN1 and PGC1α. Treatment of apoE(-/-) mice on high fat diet with paricalcitol had modest opposite effects on steatosis and gene expression. Finally, this set of genes showed concordant responses when VDR was overexpressed or silenced in HepG2 cells., Conclusions: Induced hepatocyte VDR in NAFLD regulates key hepatic lipid metabolism genes and promotes high fat diet-associated liver steatosis. Therapeutic inhibition of liver VDR may reverse steatosis in early NAFLD., Lay Summary: The amount of vitamin D receptor is induced early in the livers of mice and humans when they develop non-alcoholic fatty liver disease. If the gene for the vitamin D receptor is deleted, hepatic lipid metabolism changes and mice do not accumulate fat in the liver. We conclude that the vitamin D receptor can contribute to the fatty liver disease promoted by a high fat diet., (Copyright © 2016 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)

Published
2016
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26. Hepatitis C virus NS5A and core proteins induce oxidative stress-mediated calcium signalling alterations in hepatocytes.

Author

Dionisio N, Garcia-Mediavilla MV, Sanchez-Campos S, Majano PL, Benedicto I, Rosado JA, Salido GM, and Gonzalez-Gallego J

Subjects
Actins metabolism, Antioxidants pharmacology, Calcium Signaling drug effects, Calcium-Binding Proteins pharmacology, Cell Line, Cell Survival physiology, Cysteine Proteinase Inhibitors pharmacology, Cytokines metabolism, Hepacivirus physiology, Hepatitis C drug therapy, Hepatitis C metabolism, Hepatocytes cytology, Hepatocytes drug effects, Homeostasis drug effects, Homeostasis physiology, Humans, Oxidative Stress drug effects, Quercetin pharmacology, Reactive Nitrogen Species metabolism, Reactive Oxygen Species metabolism, Virus Replication drug effects, Virus Replication physiology, Calcium metabolism, Calcium Signaling physiology, Hepatocytes physiology, Oxidative Stress physiology, Viral Core Proteins physiology, Viral Nonstructural Proteins physiology
Abstract

Background/aims: The hepatitis C virus (HCV) structural core and non-structural NS5A proteins induce in liver cells a series of intracellular events, including elevation of reactive oxygen and nitrogen species (ROS/RNS). Since oxidative stress is associated to altered intracellular Ca(2+) homeostasis, we aimed to investigate the effect of these proteins on Ca(2+) mobilization in human hepatocyte-derived transfected cells, and the protective effect of quercetin treatment., Methods: Ca(2+) mobilization and actin reorganization were determined by spectrofluorimetry. Production of ROS/RNS was determined by flow cytometry., Results: Cells transfected with NS5A and core proteins showed enhanced ROS/RNS production and resting cytosolic Ca(2+) concentration, and reduced Ca(2+) concentration into the stores. Phenylephrine-evoked Ca(2+) release, Ca(2+) entry and extrusion by the plasma membrane Ca(2+)-ATPase were significantly reduced in transfected cells. Similar effects were observed in cytokine-activated cells. Phenylephrine-evoked actin reorganization was reduced in the presence of core and NS5A proteins. These effects were significantly prevented by quercetin. Altered Ca(2+) mobilization and increased calpain activation were observed in replicon-containing cells., Conclusions: NS5A and core proteins induce oxidative stress-mediated Ca(2+) homeostasis alterations in human hepatocyte-derived cells, which might underlie the effects of both proteins in the pathogenesis of liver disorders associated to HCV infection.

Published
2009
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27. Differential contribution of hepatitis C virus NS5A and core proteins to the induction of oxidative and nitrosative stress in human hepatocyte-derived cells.

Author

García-Mediavilla MV, Sánchez-Campos S, González-Pérez P, Gómez-Gonzalo M, Majano PL, López-Cabrera M, Clemente G, García-Monzón C, and González-Gallego J

Subjects
Cell Line, Flow Cytometry, Genes, Reporter, Humans, Inflammation, Luciferases analysis, Luciferases genetics, Models, Biological, Nitrogen Compounds, Polymerase Chain Reaction, Reactive Oxygen Species, Transfection, Hepacivirus physiology, Hepatocytes physiology, Hepatocytes virology, Nitrates metabolism, Oxidative Stress, Viral Core Proteins physiology
Abstract

Background/aims: We aimed to explore the effects of hepatitis C virus (HCV) core and NS5A proteins on reactive oxygen (ROS) and nitrogen species (RNS) formation and on gene expression profile of iNOS in human hepatocyte-derived cells., Methods: Production of ROS and RNS and nitrotyrosine residues accumulation were determined by flow cytometry and fluorescent microscopy as well as by Western blot, respectively, in NS5A- and core-transfected cells. Northern blot, Western blot, real-time PCR, and luciferase assays were used to assess iNOS gene expression in both transfectants., Results: Cytokine-activated NS5A- and core-transfected cells induced ROS and RNS production but an earlier and more marked increase was observed in NS5A-expressing cells. Superoxide production was also augmented, showing a similar temporal pattern of appearance in both NS5A- and core-transfected cells. Although both NS5A and core HCV proteins were able to up-regulate iNOS gene expression, accompanied by a nitrotyrosine-containing proteins accumulation, an earlier iNOS overexpression was observed in NS5A-expressing cells, suggesting a different time course of iNOS activation pattern for core and NS5A HCV proteins., Conclusions: Our results indicate a differential contribution of both HCV proteins to oxidative and nitrosative stress generation.

Published
2005
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