Person: Regueiro González-Barros, José Ramón
Loading...
First Name
José Ramón
Last Name
Regueiro González-Barros
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Inmunología, Oftalmología y ORL
Area
Inmunología
Identifiers
12 results
Search Results
Now showing 1 - 10 of 12
Item Virtualización de la asignatura de Inmunología(III jornada Campus Virtual UCM : Innovación en el Campus Virtual metodologías y herramientas, 2007) Cabanillas, Beatriz; Regueiro González-Barros, José Ramón; Martínez Naves, Eduardo; Recio Hoyas, María José; Gómez Del Moral Martín-Consuegra, Manuel María; Setién Baranda , Esteban Fernando; Fernández-Valmayor Crespo, Alfredo; Fernández-Pampillón Cesteros, Ana María; Merino Granizo, JorgeLa Universidad Complutense de Madrid es competitiva en docencia de Inmunología, no existiendo otra Universidad que cubra todas las diplomaturas y licenciaturas en las que hay carga docente de Inmunología [1]. Estas asignaturas, de pocos créditos pero con un temario muy denso, se beneficiarían de un soporte virtual que diera salida a muchas de las necesidades del alumno. Asimismo se ha comprobado que existe un buen material docente de Inmunología en Internet, aunque la mayoría de los contenidos se encuentran en inglés. Por ello los profesores participantes en el proyecto, con su amplia experiencia en innovación y mejora de la calidad docente [2], consideran que la Inmunología es susceptible de virtualizar con éxito.Item Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis(Cell Death and Disease, 2023) Kang, Zheng; Fengjie, Hao; Medrano García, Sandra; Chaobo, Chen; Morán Blanco, Laura; Peligros Gómez, María Isabel; Bañares Cañizares, Rafael; Vaquero Martín, Francisco Javier; Gómez Del Moral Martín-Consuegra, Manuel María; Regueiro González-Barros, José Ramón; Martínez Naves, Eduardo; Gallego Durán, Rocío; Maya, Douglas; Ampuero, Javier; Romero Gómez, Manuel; Gilbert Ramos, Albert; Guixé Muntet, Sergi; Fernández Iglesias, Anabel; Gracia Sancho, Jordi; Coll, Mar; Graupera, Isabel; Ginès, Pere; Pericàs, Juan M.; Ramos Molina, Bruno; Herranz, José María; Ávila, Matías A.; Nevzorova, Yulia; Fernández Malavé, Edgar Gonzalo; Cubero Palero, Francisco JavierProgressive hepatic damage and fibrosis are major features of chronic liver diseases of different etiology, yet the underlying molecular mechanisms remain to be fully defined. N-RAS, a member of the RAS family of small guanine nucleotide-binding proteins also encompassing the highly homologous H-RAS and K-RAS isoforms, was previously reported to modulate cell death and renal fibrosis; however, its role in liver damage and fibrogenesis remains unknown. Here, we approached this question by using N-RAS deficient (N-RAS-/-) mice and two experimental models of liver injury and fibrosis, namely carbon tetrachloride (CCl4) intoxication and bile duct ligation (BDL). In wild-type (N-RAS+/+) mice both hepatotoxic procedures augmented N-RAS expression in the liver. Compared to N-RAS+/+ counterparts, N-RAS-/- mice subjected to either CCl4 or BDL showed exacerbated liver injury and fibrosis, which was associated with enhanced hepatic stellate cell (HSC) activation and leukocyte infiltration in the damaged liver. At the molecular level, after CCl4 or BDL, N-RAS-/- livers exhibited augmented expression of necroptotic death markers along with JNK1/2 hyperactivation. In line with this, N-RAS ablation in a human hepatocytic cell line resulted in enhanced activation of JNK and necroptosis mediators in response to cell death stimuli. Of note, loss of hepatic N-RAS expression was characteristic of chronic liver disease patients with fibrosis. Collectively, our study unveils a novel role for N-RAS as a negative controller of the progression of liver injury and fibrogenesis, by critically downregulating signaling pathways leading to hepatocyte necroptosis. Furthermore, it suggests that N-RAS may be of potential clinical value as prognostic biomarker of progressive fibrotic liver damage, or as a novel therapeutic target for the treatment of chronic liver disease.- Project number: PIMCD86/23-24
Item Simulación virtual de diagnóstico de inmunodeficiencias congénitas para el asentamiento de conocimientos básicos sobre inmunología(0024) Marín Marín, Ana Victoria; Martínez Naves, Eduardo; Regueiro González-Barros, José Ramón; Tortajada Alonso, Agustín; Cubero Palero, Francisco Javier; Allende Martínez, Luis Miguel; González Granado, Luis Ignacio; Muñoz Ruiz, Miguel; Chacón Arguedas, Carlos Daniel; Fernández Megino, Rebeca; Herrero Alonso, Marta; Estévez Benito, Iván; Fernández Boraita, Julia Belén; Franco Jarava, ClaraLa inmunología es una materia transversal que trata conocimientos de biología celular, bioquímica molecular, genética y patología clínica. La docencia que reciben los alumnos de primero de Medicina en nuestra Universidad, cuyas aulas se componen de 80 alumnos aproximadamente, consta de unas 36 horas anuales en una asignatura obligatoria e impartida en el segundo periodo del curso. Dada la gran complejidad inherente en el estudio inmunología, es realmente difícil lograr el interés del grupo por la asignatura a través de las técnicas docentes clásicas. En este proyecto de innovación docente, proponemos una actividad interactiva, parcialmente virtual y con una perspectiva basico-clínica interactiva mediante la cual los alumnos participarán activamente en el diagnóstico de un total de 3 pacientes pediátricos con errores congénitos de la inmunidad durante una única sesión al final del curso. Para ello, dispondremos de 3 casos clínicos reales que describirán enfermedades frecuentes dentro de la especialidad siendo presentados concisamente con datos clínicos a través de la pantalla de la misma aula docente, y de manera simultánea lanzaremos preguntas a través de una plataforma web que permitirá que los alumnos respondan utilizando un “apodo” e individualmente empleando sus teléfonos móviles. Con cada pregunta los alumnos aprenderán a identificar conceptos claves para el diagnóstico de inmunodeficiencias que no pueden abordarse en las clases magistrales por escasez de tiempo, y a la vez autoevaluarán los conocimientos adquiridos hasta el momento. Item Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis(Cell death diseases, 2023) Kang, Zheng; Fengjie, Hao; Medrano García, Sandra; Chaobo, Chen; Morán Blanco, Laura; Peligros Gómez, María Isabel; Vaquero Martín, Francisco Javier; Bañares Cañizares, Rafael; Gómez Del Moral Martín-Consuegra, Manuel María; Regueiro González-Barros, José Ramón; Martínez Naves, Eduardo; Nevzorova, Yulia; Fernández Malavé, Edgar Gonzalo; Cubero Palero, Francisco JavierProgressive hepatic damage and fibrosis are major features of chronic liver diseases of different etiology, yet the underlying molecular mechanisms remain to be fully defined. N-RAS, a member of the RAS family of small guanine nucleotide-binding proteins also encompassing the highly homologous H-RAS and K-RAS isoforms, was previously reported to modulate cell death and renal fibrosis; however, its role in liver damage and fibrogenesis remains unknown. Here, we approached this question by using N-RAS deficient (N-RAS−/−) mice and two experimental models of liver injury and fibrosis, namely carbon tetrachloride (CCl4) intoxication and bile duct ligation (BDL). In wild-type (N-RAS+/+) mice both hepatotoxic procedures augmented N-RAS expression in the liver. Compared to N-RAS+/+ counterparts, N-RAS−/− mice subjected to either CCl4 or BDL showed exacerbated liver injury and fibrosis, which was associated with enhanced hepatic stellate cell (HSC) activation and leukocyte infiltration in the damaged liver. At the molecular level, after CCl4 or BDL, N-RAS−/− livers exhibited augmented expression of necroptotic death markers along with JNK1/2 hyperactivation. In line with this, N-RAS ablation in a human hepatocytic cell line resulted in enhanced activation of JNK and necroptosis mediators in response to cell death stimuli. Of note, loss of hepatic N-RAS expression was characteristic of chronic liver disease patients with fibrosis. Collectively, our study unveils a novel role for N-RAS as a negative controller of the progression of liver injury and fibrogenesis, by critically downregulating signaling pathways leading to hepatocyte necroptosis. Furthermore, it suggests that N-RAS may be of potential clinical value as prognostic biomarker of progressive fibrotic liver damage, or as a novel therapeutic target for the treatment of chronic liver disease.Item Abnormal liver function test in patients infected with Coronavirus (SARS-CoV-2): a retrospective Single-Center Study from Spain(Journal of Clinical Medicine, 2021) Benede Ubieto, Raquel; Estévez Vázquez, Olga; Flores Perojo, Vicente; Macías Rodríguez, Ricardo U.; Ruiz Margáin, Astrid; Martínez Naves, Eduardo; Regueiro González-Barros, José Ramón; Avila, Matías A.; Trautwein, Christian; Bañares Cañizares, Rafael; Bosch, J.; Cubero Palero, Francisco Javier; Nevzorova, YuliaThe outbreak of the novel coronavirus SARS-CoV-2 epidemic has rapidly spread and still poses a serious threat to healthcare systems worldwide. In the present study, electronic medical records containing clinical indicators related to liver injury in 799 COVID-19-confirmed patients admitted to a hospital in Madrid (Spain) were extracted and analyzed. Correlation between liver injury and disease outcome was also evaluated. Serum levels of Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Gamma-glutamyltransferase (GGT), Alkaline phosphatase (ALP), Lactate dehydrogenase (LDH) and AST/ALT ratio were elevated above the Upper Limit of Normal (ULN) in 25.73%, 49.17%, 34.62%, 24.21%, 55.84% and 75% of patients, respectively. Interestingly, significant positive correlation between LDH levels and the AST/ALT ratio with disease outcome was found. Our data showed that SARS-CoV-2 virus infection leads to mild, but significant changes in serum markers of liver injury. The upregulated LDH levels as well as AST/ALT ratios upon admission may be used as additional diagnostic characteristic for COVID-19 patients.Item Fat: Quality, or Quantity? What Matters Most for the Progression of Metabolic Associated Fatty Liver Disease (MAFLD)(Biomedicines, 2021) Estévez Vázquez, Olga; Benedé Ubieto, Raquel; Guo, Feifei; Gómez Santos, Beatriz; Aspichueta, Patricia; Reissing, Johanna; Bruns, Tony; Sanz García, Carlos; Sydor, Svenja; Bechmann, Lars P; Maranillo Alcaide, Eva; Sañudo Tejero, José Ramón; Vázquez Osorio, María Teresa; Lamas Paz, Arantza; Morán, Laura; Mazariegos, Marina S; Ciudin, Andreea; Pericàs, Juan M.; Peligros, María Isabel; Vaquero, Javier; Martínez Naves, Eduardo; Liedtke, Christian; Regueiro González-Barros, José Ramón; Trautwein, Christian; Bañares Cañizares, Rafael; Cubero Palero, Francisco Javier; Nevzorova, YuliaObjectives: Lately, many countries have restricted or even banned transfat, and palm oil has become a preferred replacement for food manufacturers. Whether palm oil is potentially an unhealthy food mainly due to its high content of saturated Palmitic Acid (PA) is a matter of debate. The aim of this study was to test whether qualitative aspects of diet such as levels of PA and the fat source are risk factors for Metabolic Syndrome (MS) and Metabolic Associated Fatty Liver Disease (MAFLD). Methods: C57BL/6 male mice were fed for 14 weeks with three types of Western diet (WD): 1. LP-WD—low concentration of PA (main fat source—corn and soybean oils); 2. HP-WD—high concentration of PA (main fat source—palm oil); 3. HP-Trans-WD—high concentration of PA (mainly transfat). Results: All types of WD caused weight gain, adipocyte enlargement, hepatomegaly, lipid metabolism alterations, and steatohepatitis. Feeding with HP diets led to more prominent obesity, hypercholesterolemia, stronger hepatic injury, and fibrosis. Only the feeding with HP-Trans-WD resulted in glucose intolerance and elevation of serum transaminases. Brief withdrawal of WDs reversed MS and signs of MAFLD. However, mild hepatic inflammation was still detectable in HP groups. Conclusions: HP and HP-Trans-WD play a crucial role in the genesis of MS and MAFLD.Item Abnormal Liver Function Test in Patients Infected with Coronavirus (SARS-CoV-2): A Retrospective Single-Center Study from Spain(Journal of Clinical Medicine, 2021) Flores Perojo, Vicente; Macías Rodríguez, Ricardo U.; Ruiz Margáin, Astrid; Regueiro González-Barros, José Ramón; Ávila, Matias A; Trautwein, Christian; Bañares Cañizares, Rafael; Bosch, Jaume; Estévez Vázquez, Olga; Martínez Naves, Eduardo; Cubero Palero, Francisco Javier; Nevzorova, Yulia; Benede Ubieto, RaquelAbstract: The outbreak of the novel coronavirus SARS-CoV-2 epidemic has rapidly spread and still poses a serious threat to healthcare systems worldwide. In the present study, electronic medical records containing clinical indicators related to liver injury in 799 COVID-19-confirmed patients admitted to a hospital in Madrid (Spain) were extracted and analyzed. Correlation between liver injury and disease outcome was also evaluated. Serum levels of Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Gamma-glutamyltransferase (GGT), Alkaline phosphatase (ALP), Lactate dehydrogenase (LDH) and AST/ALT ratio were elevated above the Upper Limit of Normal (ULN) in 25.73%, 49.17%, 34.62%, 24.21%, 55.84% and 75% of patients, respectively. Interestingly, significant positive correlation between LDH levels and the AST/ALT ratio with disease outcome was found. Our data showed that SARS-CoV-2 virus infection leads to mild, but significant changes in serum markers of liver injury. The upregulated LDH levels as well as AST/ALT ratios upon admission may be used as additional diagnostic characteristic for COVID-19 patients.Item Fat: quality or quantity? What matters most for the progression of Metabolic Associated Fatty Liver Disease (MAFLD).(Biomedicines, 2021) Estévez Vázquez, Olga; Benede Ubieto, Raquel; Sanz García, Carlos; Maranillo Alcaide, Eva; Sañudo Tejero, José Ramón; Vázquez Osorio, María Teresa; Lamas Paz, Arantza; Peligros Gómez, María Isabel; Vaquero, Javier; Martínez Naves, Eduardo; Regueiro González-Barros, José Ramónfirst_pagesettingsOrder Article Reprints Open AccessArticle Fat: Quality, or Quantity? What Matters Most for the Progression of Metabolic Associated Fatty Liver Disease (MAFLD) by Olga Estévez-Vázquez 1,2ORCID,Raquel Benedé-Ubieto 1,2,Feifei Guo 2,Beatriz Gómez-Santos 3ORCID,Patricia Aspichueta 3,4,5ORCID,Johanna Reissing 6,Tony Bruns 6ORCID,Carlos Sanz-García 2ORCID,Svenja Sydor 7ORCID,Lars P. Bechmann 7,Eva Maranillo 8,José Ramón Sañudo 8,María Teresa Vázquez 8,Arantza Lamas-Paz 2ORCID,Laura Morán 2,9,Marina S. Mazariegos 2,Andreea Ciudin 10ORCID,Juan M. Pericàs 5,11,María Isabel Peligros 12,Javier Vaquero 5,9,13ORCID,add Show full author list 1 Department of Physiology, Genetics and Microbiology, Faculty of Biology, Complutense University of Madrid, 28040 Madrid, Spain 2 Department of Immunology, Ophthalmology and ENT, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain 3 Department of Physiology, Faculty of Medicine and Nursing, University of Basque Country UPV/EHU, 48940 Leioa, Spain 4 Biocruces Health Research Institute, 48903 Barakaldo, Spain 5 Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Instituto de Salud Carlos III, 28220 Madrid, Spain 6 Department of Internal Medicine III, University Hospital RWTH Aachen, 52074 Aachen, Germany 7 Department of Internal Medicine, University Hospital Knappschaftskrankenhaus, Ruhr-University Bochum, 44801 Bochum, Germany 8 Department of Human Anatomy and Embryology, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain 9 Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), 28009 Madrid, Spain 10 Endocrinology Department, Vall d’Hebron University Hospital, Vall d’Hebron Institute for Research (VHIR), 08035 Barcelona, Spain add Show full affiliation list * Author to whom correspondence should be addressed. † These authors contributed equally to this work. Biomedicines 2021, 9(10), 1289; https://doi.org/10.3390/biomedicines9101289 Submission received: 12 August 2021 / Revised: 13 September 2021 / Accepted: 19 September 2021 / Published: 22 September 2021 (This article belongs to the Special Issue Metabolic Syndrome and NASH: From Molecular Basis to Therapy) Downloadkeyboard_arrow_down Browse Figures Review Reports Versions Notes Abstract Objectives: Lately, many countries have restricted or even banned transfat, and palm oil has become a preferred replacement for food manufacturers. Whether palm oil is potentially an unhealthy food mainly due to its high content of saturated Palmitic Acid (PA) is a matter of debate. The aim of this study was to test whether qualitative aspects of diet such as levels of PA and the fat source are risk factors for Metabolic Syndrome (MS) and Metabolic Associated Fatty Liver Disease (MAFLD). Methods: C57BL/6 male mice were fed for 14 weeks with three types of Western diet (WD): 1. LP-WD—low concentration of PA (main fat source—corn and soybean oils); 2. HP-WD—high concentration of PA (main fat source—palm oil); 3. HP-Trans-WD—high concentration of PA (mainly transfat). Results: All types of WD caused weight gain, adipocyte enlargement, hepatomegaly, lipid metabolism alterations, and steatohepatitis. Feeding with HP diets led to more prominent obesity, hypercholesterolemia, stronger hepatic injury, and fibrosis. Only the feeding with HP-Trans-WD resulted in glucose intolerance and elevation of serum transaminases. Brief withdrawal of WDs reversed MS and signs of MAFLD. However, mild hepatic inflammation was still detectable in HP groups. Conclusions: HP and HP-Trans-WD play a crucial role in the genesis of MS and MAFLD.Item Human CD3γ, but not CD3δ, haploinsufficiency differentially impairs γδ versus αβ surface TCR expression(BMC Immunology, 2013) Muñoz Ruiz, Miguel; Pérez Flores, Verónica; Garcillán Goyoaga, Beatriz De; Guardo, Alberto C.; Mazariegos, Marina S.; Takada, Hidetoshi; Allende Martínez, Luis Miguel; Kilic, Sara S.; Sanal, Ozden; Roifman, Chaim M.; López Granados, Eduardo; Recio Hoyas, María José; Martínez Naves, Eduardo; Fernández Malavé, Edgar Gonzalo; Regueiro González-Barros, José RamónBackground: The T cell antigen receptors (TCR) of αβ and γδ T lymphocytes are believed to assemble in a similar fashion in humans. Firstly, αβ or γδ TCR chains incorporatea CD3δε dimer, then a CD3γε dimer and finally a ζζ homodimer, resulting in TCR complexes with the same CD3 dimer stoichiometry. Partial reduction in the expression of the highly homologous CD3γ and CD3δ proteins would thus be expected to have a similar impact in the assembly and surface expression of both TCR isotypes. To test this hypothesis, we compared the surface TCR expression of primary αβ and γδ T cells from healthy donors carrying a single null or leaky mutation in CD3G (γ+/−) or CD3D (δ+/−, δ+/leaky) with that of normal controls. Results: Although the partial reduction in the intracellular availability of CD3γ or CD3δ proteins was comparable as a consequence of the mutations, surface TCR expression measured with anti-CD3ε antibodies was significantly more decreased in γδ than in αβ T lymphocytes in CD3γ+/− individuals, whereas CD3δ+/− and CD3δ+/leaky donors showed a similar decrease of surface TCR in both T cell lineages. Therefore, surface γδ TCR expression was more dependent on available CD3γ than surface αβ TCR expression. Conclusions: The results support the existence of differential structural constraints in the two human TCR isotypes regarding the incorporation of CD3γε and CD3δε dimers, as revealed by their discordant surface expression behaviour when confronted with reduced amounts of CD3γ, but not of the homologous CD3δ chain. A modified version of the prevailing TCR assembly model is proposed to accommodate these new data.Item gd T lymphocytes in the diagnosis of human T cell receptor immunodeficiencies(Frontiers in immunology, 2015) Garcillán Goyoaga, Beatriz de; Marín Marín, Ana Victoria; Jiménez Reinoso, Anaïs; Briones Contreras, Alejandro; Muñoz Ruiz, Miguel; García León, María J; Gil Calle, Juana Nelly; Allende Martínez, Luis Miguel; Martínez Naves, Eduardo; Toribio, Maria Luisa; Regueiro González-Barros, José RamónHuman T cell receptor (TCR) immunodeficiencies (TCRID) are rare autosomal recessive disorders caused by mutations affecting TCR, CD3, or CD247 chains, which share developmental, functional, and TCR expression defects (1). Their rapid diagnosis is fundamental for patient survival and early hematopoietic stemcell transplantation.Here,we propose that studying gd T cells, which are often neglected, can be helpful for a timely diagnosis. We thus offer a diagnostic flowchart and some lab tricks based on published cases.