ArticleJournal of lipid research2010
Cholesterol loading in macrophages stimulates formation of ER-derived vesicles with elevated ACAT1 activity.
Article in Journal of lipid research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Macrophage ACAT1 Aggravates Alcohol-Associated Liver Disease by Inducing Mitochondrial Damage and NLRP3 Activation.Journal of gastroenterology and hepatology · 2026Article
- 3D cryoimaging of cell-mediated cholesterol crystal clearance in human atherosclerotic lesions.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Myeloid ACAT1/SOAT1: a novel regulator of dyslipidemia and retinal neovascularization.npj metabolic health and disease · 2025Review
- Nanoparticle-based itaconate treatment recapitulates low-cholesterol/low-fat diet-induced atherosclerotic plaque resolution.Cell reports · 2024Article
- Role of acyl-coenzyme A: cholesterol transferase 1 (ACAT1) in retinal neovascularization.Journal of neuroinflammation · 2023Article
- Reversible translocation of acyl-CoA:cholesterol acyltransferase (ACAT) between the endoplasmic reticulum and vesicular structures.Frontiers in molecular biosciences · 2023Article
- Nanodisc scaffold peptide (NSPArchives of biochemistry and biophysics · 2020Article
- Adenovirus Reveals New Pathway for Cholesterol Egress from the Endolysosomal System.International journal of molecular sciences · 2020Review
- Retinal Hypercholesterolemia Triggers Cholesterol Accumulation and Esterification in Photoreceptor Cells.The Journal of biological chemistry · 2016Article
- Myeloid Acyl-CoA:Cholesterol Acyltransferase 1 Deficiency Reduces Lesion Macrophage Content and Suppresses Atherosclerosis Progression.The Journal of biological chemistry · 2016Article
- ABCA1-dependent sterol release: sterol molecule specificity and potential membrane domain for HDL biogenesis.Journal of lipid research · 2016Article
- ACAT1-associated Late Endosomes/Lysosomes Significantly Improve Impaired Intracellular Cholesterol Metabolism and the Survival of Niemann-Pick Type C Mice.Acta histochemica et cytochemica · 2014Article
- Bis(monoacylglycero)phosphate accumulation in macrophages induces intracellular cholesterol redistribution, attenuates liver-X receptor/ATP-Binding cassette transporter A1/ATP-binding cassette transporter G1 pathway, and impairs cholesterol efflux.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Apolipoprotein A-I Helsinki promotes intracellular acyl-CoA cholesterol acyltransferase (ACAT) protein accumulation.Molecular and cellular biochemistry · 2013Article
- Characterizing virulence-specific perturbations in the mitochondrial function of macrophages infected with Mycobacterium tuberculosis.Scientific reports · 2013Article
- Subcellular localization and regulation of StarD4 protein in macrophages and fibroblasts.Biochimica et biophysica acta · 2011Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
ACAT1 is normally a resident enzyme in the endoplasmic reticulum (ER). We previously showed that treating macrophages with denatured LDL causes a large increase in ER-derived, ACAT1-positive vesicles. Here, we isolated ER membranes and ER-derived vesicles to examine their ACAT enzyme activity in vitro. The results showed that when macrophages are grown under normal conditions, ACAT1 is located in high density ER membrane; its enzymatic activity is relatively low. Loading macrophages with cholesterol did not increase the total cellular ACAT1 protein content significantly but caused more ACAT1 to appear in ER-derived vesicles. These vesicles exhibit lower density and are associated with markers of both ER and the trans-Golgi network. When normalized with equal ACAT1 protein mass, the enzymatic activities of ACAT1 in ER-derived vesicles were 3-fold higher than those present in ER membrane. Results using reconstituted ACAT enzyme assay showed that the increase in enzyme activity in ER-derived vesicles is not due to an increase in the cholesterol content associated with these vesicles. Overall, our results show that macrophages cope with cholesterol loading by using a novel mechanism: they produce more ER-derived vesicles with elevated ACAT1 enzyme activity without having to produce more ACAT1 protein.
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Registered trials
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.