Autor según el artículo: Rodríguez-Calvo, R; Guardiola, M; Oliva, I; Arrando, H; Arranz, I; Ferré, A; Pellicer, P; Parra, S; Ribalta, J; Castro, A
Departamento: Medicina i Cirurgia
Autor/es de la URV: Arranz De La Calle, Isabel / Castro Salomó, Antoni / Guardiola Guionnet, Montserrat / Oliva Rodríguez, Iris / Parra Pérez, Sandra / Ribalta Vives, Josep / Rodríguez Calvo, Ricardo
Palabras clave: Systemic-lupus-erythematosus Sle Low-density lipoprotein Endothelial cells Cardiovascular disease subclasses risk low-density lipoprotein endothelial cells coronary-heart-disease cardiovascular disease accelerated atherosclerosis
Resumen: © The Author(s) 2020. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please email: journals.permissions@oup.com. OBJECTIVES: SLE patients have an enhanced risk of atherosclerosis and cardiovascular disease. However, the increased prevalence of cardiovascular disease is not fully explained by traditional Framingham cardiovascular risk factors. Specific features of low-density lipoprotein (LDL) particles, other than plasma concentration, may induce accelerated atherosclerosis at early stages in these patients. Thus, we aimed to explore the impact of LDL from both active and inactive SLE patients on human aortic endothelial cells. METHODS: Human aortic endothelial cells were stimulated with the same concentration of LDL particles isolated from pooled serum that was collected from 13 SLE patients during both active and inactive states. Gene expression and cell migration assays were performed. RESULTS: Circulating LDL particles obtained from healthy volunteers and SLE patients in both remission and flare states were comparable in terms of number, cholesterol and triglyceride content, and net electric charge. Stimulation of cells with LDL from active SLE patients induced the expression of vascular cell adhesion molecule 1 (∼2.0-fold, P < 0.05), monocyte chemoattractant protein 1 (∼2.0-fold, P < 0.05) and matrix metallopeptidase 2 (∼1.6-fold, P < 0.01) compared with cells stimulated with LDL from inactive SLE patients. Additionally, LDL extracted from active patients increased cell migration in a wound-healing assay (1.4-fold, P < 0.05). CONCLUSION: Our data show that, at the same LDL concentration, LDL from active SLE patients had increased proatherogenic effects on endothelial cells compared with LDL from the same patients when in an inactive or remission state.
Áreas temáticas: Saúde coletiva Rheumatology Pharmacology (medical) Odontología Medicina iii Medicina ii Medicina i Interdisciplinar General medicine Farmacia Ensino Ciências biológicas iii Ciências biológicas ii Ciências biológicas i Ciência de alimentos Biotecnología
Acceso a la licencia de uso: https://creativecommons.org/licenses/by/3.0/es/
Direcció de correo del autor: ricardo.rodriguez@urv.cat isabel.arranz@estudiants.urv.cat sandra.parra@urv.cat antoni.castro@urv.cat montse.guardiola@urv.cat josep.ribalta@urv.cat
Identificador del autor: 0000-0001-9363-6574 0000-0001-5441-6333 0000-0002-9696-7384 0000-0002-8879-4719
Fecha de alta del registro: 2024-07-27
Versión del articulo depositado: info:eu-repo/semantics/submittedVersion
Enlace a la fuente original: https://academic.oup.com/rheumatology/article-abstract/60/2/866/5897208?redirectedFrom=fulltext
URL Documento de licencia: https://repositori.urv.cat/ca/proteccio-de-dades/
Referencia al articulo segun fuente origial: Rheumatology. 60 (2): 866-871
Referencia de l'ítem segons les normes APA: Rodríguez-Calvo, R; Guardiola, M; Oliva, I; Arrando, H; Arranz, I; Ferré, A; Pellicer, P; Parra, S; Ribalta, J; Castro, A (2021). Low-density lipoprotein from active SLE patients is more atherogenic to endothelial cells than low-density lipoprotein from the same patients during remission. Rheumatology, 60(2), 866-871. DOI: 10.1093/rheumatology/keaa380
DOI del artículo: 10.1093/rheumatology/keaa380
Entidad: Universitat Rovira i Virgili
Año de publicación de la revista: 2021
Tipo de publicación: Journal Publications
Repositori URV