ArticleArteriosclerosis, thrombosis, and vascular biology2013
Physiological difference in autophagic flux in macrophages from 2 mouse strains regulates cholesterol ester metabolism.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Discussion on the comparison of Raman spectroscopy and cardiovascular disease-related imaging techniques and the future applications of Raman technology: a systematic review.Lasers in medical science · 2025Pooled it
- Optimized Method to Generate Well-Characterized Macrophages from Induced Pluripotent Stem Cells.Biomedicines · 2025Article
- A novel therapeutic strategy for atherosclerosis: autophagy-dependent cholesterol efflux.Journal of physiology and biochemistry · 2022Review
- Off-target effects of the lysosomal acid lipase inhibitors Lalistat-1 and Lalistat-2 on neutral lipid hydrolases.Molecular metabolism · 2022Article
- Article
- Quantitative trait locus mapping identifies the Gpnmb gene as a modifier of mouse macrophage lysosome function.Scientific reports · 2021Article
- Traditional Chinese Medication Tongxinluo Attenuates Lipidosis in Ox-LDL-Stimulated Macrophages by Enhancing Beclin-1-Induced Autophagy.Frontiers in pharmacology · 2021Article
- Soat1 mediates the mouse strain effects on cholesterol loading-induced endoplasmic reticulum stress and CHOP expression in macrophages.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2021Article
- PCSK9 deficiency reduces atherosclerosis, apolipoprotein B secretion, and endothelial dysfunction.Journal of lipid research · 2018Article
- Quantitative Trait Locus Mapping of Macrophage Cholesterol Metabolism and CRISPR/Cas9 Editing Implicate an ACAT1 Truncation as a Causal Modifier Variant.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Lysosome-mediated degradation of a distinct pool of lipid droplets during hepatic stellate cell activation.The Journal of biological chemistry · 2017Article
- microRNA-33 Regulates Macrophage Autophagy in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Hypericin-mediated sonodynamic therapy induces autophagy and decreases lipids in THP-1 macrophage by promoting ROS-dependent nuclear translocation of TFEB.Cell death & disease · 2016Article
- ORMDL orosomucoid-like proteins are degraded by free-cholesterol-loading-induced autophagy.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Self-eating in the plaque: what macrophage autophagy reveals about atherosclerosis.Trends in endocrinology and metabolism: TEM · 2014Review
- MicroRNA control of high-density lipoprotein metabolism and function.Circulation research · 2014Review
- Acute sterol o-acyltransferase 2 (SOAT2) knockdown rapidly mobilizes hepatic cholesterol for fecal excretion.PloS one · 2014Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveDBA/2 apoE(-/-) mice have ≈10-fold larger lesions than AKR apoE(-/-) mice. The objective of this study was to determine whether macrophages from these 2 strains had altered cholesterol metabolism that might play a role in their divergent atherosclerosis susceptibility. APPROACH AND
resultsAKR and DBA/2 macrophages incubated with acetylated low-density lipoprotein resulted in higher cholesterol ester (CE) and lower free cholesterol accumulation in the DBA/2 cells. However, these strains had equivalent acetylated low-density lipoprotein uptake and cholesterol esterification activity. Cholesterol efflux from unloaded cells to apolipoprotein A-I or high-density lipoprotein was similar in the 2 strains. However, on acetylated low-density lipoprotein loading, cholesterol efflux was impaired in the DBA/2 cells, but this impairment was corrected by loading in the presence of an inhibitor of cholesterol esterification. Thus, the cholesterol efflux capabilities are similar in these strains, but there seemed to be a defect in lipid droplet-stored CE mobilization in DBA/2 cells. Lalistat 1, a specific inhibitor of lysosomal acid lipase, completely blocked the hydrolysis of lipid droplet-stored CE, implying that lipid droplet autophagy is responsible for CE turnover in these cells. CE turnover was 2-fold slower in DBA/2 versus AKR cells. Autophagic flux, estimated by a fluorescent light chain 3-II reporter and the increase in p62 levels after chloroquine treatment, was higher in AKR versus DBA/2 macrophages, which had an apparent decrease in autophagosome fusion with lysosomes. When autophagy was activated by amino acid starvation, CE levels decreased in DBA/2 cells.
conclusionsPhysiological regulation of autophagy in macrophages controls CE accumulation and may modify atherosclerosis susceptibility.
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