Please use this identifier to cite or link to this item: http://hdl.handle.net/10668/410
Title: High ACSL5 transcript levels associate with systemic lupus erythematosus and apoptosis in Jurkat T lymphocytes and peripheral blood cells
Authors: Catalá-Rabasa, Antonio
Ndagire, Dorothy
Sabio, Jose Mario
Fedetz, María
Matesanz, Fuencisla
Alcina, Antonio
metadata.dc.contributor.authoraffiliation: [Catalá-Rabasa,A; Ndagire,D; Fedetz,M; Matesanz,F; Alcina,A] Department of Cell Biology and Immunology, Instituto de Parasitología y Biomedicina “López Neyra”- Consejo Superior de Investigaciones Científicas (IPBLN-CSIC), Granada, Spain. [Sabio,JM] Unidad de Enfermedades Autoinmunes Sistémicas, Servicio de Medicina Interna, Hospital Universitario Virgen de las Nieves, Granada, Spain.
Keywords: Biología Celular;Biología Computacional;Genómica;Genética;Alergia e Inmunología;Biología Molecular;Reumatología;Cell Biology;Computational Biology;Genetics and Genomics;Immunology;Molecular Biology;Rheumatology
metadata.dc.subject.mesh: Medical Subject Headings::Diseases::Immune System Diseases::Autoimmune Diseases::Lupus Erythematosus, Systemic
Medical Subject Headings::Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis
Medical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Coenzymes::Coenzyme A::Acyl Coenzyme A
Issue Date: 6-Dec-2011
Publisher: Public Library of Science
Citation: Catalá-Rabasa A, Ndagire D, Sabio JM, Fedetz M, Matesanz F, Alcina A. High ACSL5 Transcript Levels Associate with Systemic Lupus Erythematosus and Apoptosis in Jurkat T Lymphocytes and Peripheral Blood Cells. PLoS ONE .2011 ; 6(12): e28591.
Abstract: BACKGROUND: Systemic lupus erythematosus (SLE) is a prototypical autoimmune disease in which increased apoptosis and decreased apoptotic cells removal has been described as most relevant in the pathogenesis. Long-chain acyl-coenzyme A synthetases (ACSLs) have been involved in the immunological dysfunction of mouse models of lupus-like autoimmunity and apoptosis in different in vitro cell systems. The aim of this work was to assess among the ACSL isoforms the involvement of ACSL2, ACSL4 and ACSL5 in SLE pathogenesis. FINDINGS: With this end, we determined the ACSL2, ACSL4 and ACSL5 transcript levels in peripheral blood mononuclear cells (PBMCs) of 45 SLE patients and 49 healthy controls by quantitative real time-PCR (q-PCR). We found that patients with SLE had higher ACSL5 transcript levels than healthy controls [median (range), healthy controls =16.5 (12.3-18.0) vs. SLE = 26.5 (17.8-41.7), P = 3.9x10 E-5] but no differences were found for ACSL2 and ACSL4. In in vitro experiments, ACSL5 mRNA expression was greatly increased when inducing apoptosis in Jurkat T cells and PBMCs by Phorbol-Myristate-Acetate plus Ionomycin (PMA+Io). On the other hand, short interference RNA (siRNA)-mediated silencing of ACSL5 decreased induced apoptosis in Jurkat T cells up to the control levels as well as decreased mRNA expression of FAS, FASLG and TNF. CONCLUSIONS: These findings indicate that ACSL5 may play a role in the apoptosis that takes place in SLE. Our results point to ACSL5 as a potential novel functional marker of pathogenesis and a possible therapeutic target in SLE
URI: http://hdl.handle.net/10668/410
metadata.dc.relation.publisherversion: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0028591
metadata.dc.identifier.doi: 10.1371/journal.pone.0028591
ISSN: 1932-6203 (Online)
Appears in Collections:01- Artículos - Hospital Virgen de las Nieves

Files in This Item:
File Description SizeFormat 
Sabio_HighACSL5.pdfArtículo principal506,61 kBAdobe PDFView/Open


This item is protected by original copyright



This item is licensed under a Creative Commons License Creative Commons