ArticleJournal of cell science2016
LPS impairs oxygen utilization in epithelia by triggering degradation of the mitochondrial enzyme Alcat1.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- FBXO28 suppresses liver cancer invasion and metastasis by promoting PKA-dependent SNAI2 degradation.Oncogene · 2023Article
- Protein arginine N-methyltransferase 4 (PRMT4) contributes to lymphopenia in experimental sepsis.Thorax · 2023Article
- Cardioprotection Attributed to Aerobic Exercise-Mediated Inhibition of ALCAT1 and Oxidative Stress-Induced Apoptosis in MI Rats.Biomedicines · 2022Article
- Porcine Deltacoronavirus Infection Cleaves HDAC2 to Attenuate Its Antiviral Activity.Journal of virology · 2022Article
- Patient Stratification in Sepsis: Using Metabolomics to Detect Clinical Phenotypes, Sub-Phenotypes and Therapeutic Response.Metabolites · 2022Review
- Role of Lysocardiolipin Acyltransferase in Cigarette Smoke-Induced Lung Epithelial Cell Mitochondrial ROS, Mitochondrial Dynamics, and Apoptosis.Cell biochemistry and biophysics · 2022Article
- Past Experiences for Future Applications of Metabolomics in Critically Ill Patients with Sepsis and Septic Shocks.Metabolites · 2021Review
- Histone Deacetylase Inhibition Regulates Lipid Homeostasis in a Mouse Model of Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2021Article
- Endotoxin stabilizes protein arginine methyltransferase 4 (PRMT4) protein triggering death of lung epithelia.Cell death & disease · 2021Article
- Neurodevelopmental Disorders (NDD) Caused by Genomic Alterations of the Ubiquitin-Proteasome System (UPS): the Possible Contribution of Immune Dysregulation to Disease Pathogenesis.Frontiers in molecular neuroscience · 2021Review
- Anti-Inflammatory Potential of Cultured Ginseng Roots Extract in Lipopolysaccharide-Stimulated Mouse Macrophages and Adipocytes.International journal of environmental research and public health · 2020Article
- Cigarette smoke extract modulatesAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
- LPS promotes HBO1 stability via USP25 to modulate inflammatory gene transcription in THP-1 cells.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018Article
- Lipopolysaccharide modulates p300 and Sirt1 to promote PRMT1 stability via an SCFJournal of cell science · 2017Article
- Oxidative stress destabilizes protein arginine methyltransferase 4 via glycogen synthase kinase 3β to impede lung epithelial cell migration.American journal of physiology. Cell physiology · 2017Article
- Proteomic Analysis of HDAC3 Selective Inhibitor in the Regulation of Inflammatory Response of Primary Microglia.Neural plasticity · 2017Article
- Psychomotor retardation with a 1q42.11-q42.12 deletion.Hereditas · 2017Article
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Authors and funding
17 authors at 2 institutions in 2 countries.
Funding
Abstract
Cardiolipin (also known as PDL6) is an indispensable lipid required for mitochondrial respiration that is generated through de novo synthesis and remodeling. Here, the cardiolipin remodeling enzyme, acyl-CoA:lysocardiolipin-acyltransferase-1 (Alcat1; SwissProt ID, Q6UWP7) is destabilized in epithelia by lipopolysaccharide (LPS) impairing mitochondrial function. Exposure to LPS selectively decreased levels of carbon 20 (C20)-containing cardiolipin molecular species, whereas the content of C18 or C16 species was not significantly altered, consistent with decreased levels of Alcat1. Alcat1 is a labile protein that is lysosomally degraded by the ubiquitin E3 ligase Skp-Cullin-F-box containing the Fbxo28 subunit (SCF-Fbxo28) that targets Alcat1 for monoubiquitylation at residue K183. Interestingly, K183 is also an acetylation-acceptor site, and acetylation conferred stability to the enzyme. Histone deacetylase 2 (HDAC2) interacted with Alcat1, and expression of a plasmid encoding HDAC2 or treatment of cells with LPS deacetylated and destabilized Alcat1, whereas treatment of cells with a pan-HDAC inhibitor increased Alcat1 levels. Alcat1 degradation was partially abrogated in LPS-treated cells that had been silenced for HDAC2 or treated with MLN4924, an inhibitor of Cullin-RING E3 ubiquitin ligases. Thus, LPS increases HDAC2-mediated Alcat1 deacetylation and facilitates SCF-Fbxo28-mediated disposal of Alcat1, thus impairing mitochondrial integrity.
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