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Your search keyword '"Ester López-Gallardo"' showing total 2 results
Start Over Author "Ester López-Gallardo" Publisher elsevier
2 results on '"Ester López-Gallardo"'

1. Pharmacologic concentrations of linezolid modify oxidative phosphorylation function and adipocyte secretome

Author

Laura Llobet, M. Pilar Bayona-Bafaluy, David Pacheu-Grau, Elena Torres-Pérez, José M. Arbones-Mainar, M. Ángeles Navarro, Covadonga Gómez-Díaz, Julio Montoya, Ester López-Gallardo, and Eduardo Ruiz-Pesini

Subjects
Linezolid, Oxidative phosphorylation, Adipocyte, Secretome, Apolipoprotein E, Adipokine, Medicine (General), R5-920, Biology (General), QH301-705.5
Abstract

The oxidative phosphorylation system is important for adipocyte differentiation. Therefore, xenobiotics inhibitors of the oxidative phosphorylation system could affect adipocyte differentiation and adipokine secretion. As adipokines impact the overall health status, these xenobiotics may have wide effects on human health. Some of these xenobiotics are widely used therapeutic drugs, such as ribosomal antibiotics. Because of its similarity to the bacterial one, mitochondrial translation system is an off-target for these compounds. To study the influence of the ribosomal antibiotic linezolid on adipokine production, we analyzed its effects on adipocyte secretome. Linezolid, at therapeutic concentrations, modifies the levels of apolipoprotein E and several adipokines and proteins related with the extracellular matrix. This antibiotic also alters the global methylation status of human adipose tissue-derived stem cells and, therefore, its effects are not limited to the exposure period. Besides their consequences on other tissues, xenobiotics acting on the adipocyte oxidative phosphorylation system alter apolipoprotein E and adipokine production, secondarily contributing to their systemic effects.

Published
2017
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2. Coenzyme Q10 deficiency in mitochondrial DNA depletion syndromes

Author

Ester López-Gallardo, Plácido Navas, Belén Pérez-Dueñas, Raquel Montero, John M. Land, Cristina Jou, Cecilia Jimenez, Angels García-Cazorla, Rafael Artuch, Cândida Mendes, Manuela Grazina, Luísa Diogo, Marta Simões, Aleix Navarro-Sastre, Maria del Mar O’Callaghan, Julio Montoya, Maria João Santos, Iain P. Hargreaves, Nuria Buján, Eduardo Ruiz-Pesini, Mercè Pineda, Andrés Nascimento, Paz Briones, Carl Fratter, Paula Garcia, Leonardo Salviati, Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación (España), European Commission, Centro de Investigación Biomédica en Red Enfermedades Raras (España), Gobierno de Aragón, University College London, Asociación de Enfermos de Patologías Mitocondriales (España), and National Institute for Health Research (UK)

Subjects
Coenzyme Q10, Mitochondrial DNA, medicine.medical_specialty, Mitochondrial disorders, Mitochondrial disease, food and beverages, Cell Biology, Disease, Biology, medicine.disease, Molecular biology, Pathophysiology, chemistry.chemical_compound, Endocrinology, Coenzyme Q10 deficiency, chemistry, Internal medicine, Coenzyme Q – cytochrome c reductase, hemic and lymphatic diseases, Mitochondrial DNA depletion syndrome, medicine, Molecular Medicine, Molecular Biology
Abstract

Coenzyme Q10 deficiency study group et al., We evaluated coenzyme Q10 (CoQ) levels in patients studied under suspicion of mitochondrial DNA depletion syndromes (MDS) (n = 39). CoQ levels were quantified by HPLC, and the percentage of mtDNA depletion by quantitative real-time PCR. A high percentage of MDS patients presented with CoQ deficiency as compared to other mitochondrial patients (Mann–Whitney-U test: p = 0.001). Our findings suggest that MDS are frequently associated with CoQ deficiency, as a possible secondary consequence of disease pathophysiology. Assessment of muscle CoQ status seems advisable in MDS patients since the possibility of CoQ supplementation may then be considered as a candidate therapy., This work has been supported by grant from the Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación, Spain (FIS: PI11/00078, PI10/00662, PI11/01301, PI08/0307 and PI08/0663 and a Fellowship to IMR PI07/00184). The Centro de Investigaciones Biomédicas en Red de Enfermedades Raras (CIBERER) is an initiative of the Instituto de Salud Carlos III by Departamento de Ciencia, Tecnología y Universidad del Gobierno de Aragón y Fondo Social Europeo (Grupo B33) and Asociación de Enfermos de Patología Mitocondrial (AEPMI). Part of this work was undertaken at UCLH which received a proportion of funding from the Department of Health's NIHR Biomedical Research Centres funding scheme.

Published
2013

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