ArticlePloS one2011
High ACSL5 transcript levels associate with systemic lupus erythematosus and apoptosis in Jurkat T lymphocytes and peripheral blood cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 16 citations in OpenAlex.
- The multifaceted roles of the ACSL family in cancer: Metabolic reprogramming, ferroptosis regulation and tumour immune microenvironment remodelling.Clinical and translational medicine · 2026Review
- ACSL5 programs fatty acid metabolism and mitochondrial fitness to sustain pathogenic T cells and exacerbate Sjögren's syndrome.International journal of biological sciences · 2026Article
- Effects of interleukin-23 on the activation of mucosal-associated invariant T cells from oral lichen planus.The Journal of international medical research · 2023Article
- Splice-site variant in ACSL5: a marker promoting opposing effect on cell viability and protein expression.European journal of human genetics : EJHG · 2019Article
- Article
- The effect of acyl-CoA synthetase long-chain family member 5 on triglyceride synthesis in bovine preadipocytes.Archives animal breeding · 2019Article
- Long-Chain Acyl-CoA Synthetase 1 Role in Sepsis and Immunity: Perspectives From a Parallel Review of Public Transcriptome Datasets and of the Literature.Frontiers in immunology · 2019Review
- Effect of Jieduquyuziyin prescription-treated rat serum on MeCP2 gene expression in Jurkat T cells.In vitro cellular & developmental biology. Animal · 2018Article
- Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells.Canadian journal of gastroenterology & hepatology · 2017Article
- A splice variant in the ACSL5 gene relates migraine with fatty acid activation in mitochondria.European journal of human genetics : EJHG · 2016Article
- Long-chain acyl-CoA synthetase in fatty acid metabolism involved in liver and other diseases: an update.World journal of gastroenterology · 2015Review
- Fus1/Tusc2 is a novel regulator of mitochondrial calcium handling, Ca2+-coupled mitochondrial processes, and Ca2+-dependent NFAT and NF-κB pathways in CD4+ T cells.Antioxidants & redox signaling · 2014Article
- PMA and ionomycin induce glioblastoma cell death: activation-induced cell-death-like phenomena occur in glioma cells.PloS one · 2013Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSystemic 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.
findingsWith 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 = 3.9×10 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.
conclusionsThese 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.
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