ArticleJournal of lipid research2009
TNF-alpha stimulates the ACAT1 expression in differentiating monocytes to promote the CE-laden cell formation.
Article in Journal of lipid research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 72 citations in OpenAlex.
- Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis.Reviews in cardiovascular medicine · 2025Review
- Myeloid ACAT1/SOAT1: a novel regulator of dyslipidemia and retinal neovascularization.npj metabolic health and disease · 2025Review
- Mechanism and therapeutic potential of liver injury induced by cholesterol-associated proteins.Frontiers in pharmacology · 2025Review
- ACAT1/SOAT1 Blockade Suppresses LPS-Mediated Neuroinflammation by Modulating the Fate of Toll-like Receptor 4 in Microglia.International journal of molecular sciences · 2023Article
- Crosstalk between cholesterol metabolism and psoriatic inflammation.Frontiers in immunology · 2023Review
- Targeting sterol-O-acyltransferase 1 to disrupt cholesterol metabolism for cancer therapy.Frontiers in oncology · 2023Review
- The effect of ox-LDL and platelets on macrophages, M2 macrophage polarization, and foam cell formation.ARYA atherosclerosis · 2023Article
- Sterol O-Acyltransferase Inhibition Ameliorates High-Fat Diet-Induced Renal Fibrosis and Tertiary Lymphoid Tissue Maturation after Ischemic Reperfusion Injury.International journal of molecular sciences · 2022Article
- Reprogramming cholesterol metabolism in macrophages and its role in host defense against cholesterol-dependent cytolysins.Cellular & molecular immunology · 2022Review
- Blocking cholesterol storage to treat Alzheimer's disease.Exploration of neuroprotective therapy · 2021Article
- Ischemic Heart Disease and Rheumatoid Arthritis-Two Conditions, the Same Background.Life (Basel, Switzerland) · 2021Review
- TNFα-Induced LDL Cholesterol Accumulation Involve Elevated LDLR Cell Surface Levels and SR-B1 Downregulation in Human Arterial Endothelial Cells.International journal of molecular sciences · 2021Article
- Serum levels of IL-32 in patients with coronary artery disease and its relationship with the serum levels of IL-6 and TNF-α.Molecular biology reports · 2021Article
- RORα Regulates Cholesterol Metabolism of CD8Cancers · 2020Article
- Mechanisms and regulation of cholesterol homeostasis.Nature reviews. Molecular cell biology · 2020Review
- Dysregulation of Neuronal Cholesterol Homeostasis upon Exposure to HIV-1 Tat and Cocaine Revealed by RNA-Sequencing.Scientific reports · 2018Article
- Storage lipid studies in tuberculosis reveal that foam cell biogenesis is disease-specific.PLoS pathogens · 2018Article
- Dietary compounds have potential in controlling atherosclerosis by modulating macrophage cholesterol metabolism and inflammation via miRNA.NPJ science of food · 2018Review
- New Insights into the Immunobiology of Mononuclear Phagocytic Cells and Their Relevance to the Pathogenesis of Cardiovascular Diseases.Frontiers in immunology · 2017Review
- Low-level expression of human ACAT2 gene in monocytic cells is regulated by the C/EBP transcription factors.Acta biochimica et biophysica Sinica · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
High levels of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) are present in atherosclerotic lesions. TNF-alpha regulates expression of multiple genes involved in various stages of atherosclerosis, and it exhibits proatherosclerotic and antiatherosclerotic properties. ACAT catalyzes the formation of cholesteryl esters (CE) in monocytes/macrophages, and it promotes the foam cell formation at the early stage of atherosclerosis. We hypothesize that TNF-alpha may be involved in regulating the ACAT gene expression in monocytes/macrophages. In this article, we show that in cultured, differentiating human monocytes, TNF-alpha enhances the expression of the ACAT1 but not ACAT2 gene, increases the cholesteryl ester accumulation, and promotes the lipid-laden cell formation. Several other proinflammatory cytokines tested do not affect the ACAT1 gene expression. The stimulation effect is consistent with a receptor-dependent process, and is blocked by using nuclear factor-kappa B (NF-kappa B) inhibitors. A functional and unique NF-kappa B element located within the human ACAT1 gene proximal promoter is required to mediate the action of TNF-alpha. Our data demonstrate that TNF-alpha, through the NF-kappa B pathway, specifically enhances the expression of human ACAT1 gene to promote the CE-laden cell formation from the differentiating monocytes, and our data support the hypothesis that TNF-alpha is proatherosclerotic during early phase of lesion development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.