ArticleProceedings of the National Academy of Sciences of the United States of America1998
Low-dose expression of a human apolipoprotein E transgene in macrophages restores cholesterol efflux capacity of apolipoprotein E-deficient mouse plasma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 75 citations in OpenAlex.
- Review
- APOE Lipoprotein Particles: Pathophysiology, Therapy, and the Crosstalk in Alzheimer's Disease and Cardiovascular Disease.Molecular neurobiology · 2025Review
- Dysfunctional high-density lipoprotein: an updated review.Frontiers in cardiovascular medicine · 2025Review
- Interactions Between HDL and CD4+ T Cells: A Novel Understanding of HDL Anti-Inflammatory Properties.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Correlations between the NMR Lipoprotein Profile,International journal of molecular sciences · 2023Article
- Apolipoprotein E in Cardiometabolic and Neurological Health and Diseases.International journal of molecular sciences · 2022Review
- ApoE Lipidation as a Therapeutic Target in Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Current and Emerging Reconstituted HDL-apoA-I and HDL-apoE Approaches to Treat Atherosclerosis.Journal of personalized medicine · 2018Review
- Modulation of autoimmune arthritis severity in mice by apolipoprotein E (ApoE) and cholesterol.Clinical and experimental immunology · 2016Article
- ApoE knockout and knockin mice: the history of their contribution to the understanding of atherogenesis.Journal of lipid research · 2016Article
- Anti-inflammatory and cholesterol-reducing properties of apolipoprotein mimetics: a review.Journal of lipid research · 2014Review
- Type VIII collagen mediates vessel wall remodeling after arterial injury and fibrous cap formation in atherosclerosis.The American journal of pathology · 2013Article
- Article
- Activation of the TLR4 signaling pathway and abnormal cholesterol efflux lead to emphysema in ApoE-deficient mice.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Macrophage-specific apoE gene repair reduces diet-induced hyperlipidemia and atherosclerosis in hypomorphic Apoe mice.PloS one · 2012Article
- Effect of rosiglitazone on HDL metabolism in subjects with metabolic syndrome and low HDL.Journal of lipid research · 2011Article
- Triacylglycerol-rich lipoproteins alter the secretion, and the cholesterol-effluxing function, of apolipoprotein E-containing lipoprotein particles from human (THP-1) macrophages.The Biochemical journal · 2001Article
- Dissection of the complex role of apolipoprotein E in lipoprotein metabolism and atherosclerosis using mouse models.Current atherosclerosis reports · 1999Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoprotein E- (apoE) deficient (E-/-) mice develop severe hyperlipidemia and diffuse atherosclerosis. Low-dose expression of a human apoE3 transgene in macrophages of apoE-deficient mice (E-/-hTgE+/0), which results in about 5% of wild-type apoE plasma levels, did not correct hyperlipidemia but significantly reduced the extent of atherosclerotic lesions. To investigate the contribution of apoE to reverse cholesterol transport, we compared plasmas of wild-type (E+/+), E-/-, and E-/-hTgE+/0 mice for the appearance of apoE-containing lipoproteins by electrophoresis and their capacity to take up and esterify 3H-labeled cholesterol from radiolabeled fibroblasts or J774 macrophages. Wild-type plasma displayed lipoproteins containing apoE that were the size of high density lipoprotein and that had either electrophoretic alpha or gamma mobilities. Similar particles were also present in E-/-hTgE+/0 plasma. Depending on incubation time, E-/- plasma released 48-74% less 3H-labeled cholesterol from fibroblasts than E+/+ plasma, whereas cholesterol efflux into E-/-hTgE+/0 plasma was only 11-25% lower than into E+/+ plasma. E-/-hTgE+/0 plasma also released 10% more 3H-labeled cholesterol from radiolabeled J774 macrophages than E-/- plasma. E+/+ and E-/-hTgE+/0 plasma each esterified significantly more cell-derived 3H-labeled cholesterol than E-/- plasma. Moreover, E-/- plasma accumulated much smaller proportions of fibroblast-derived 3H-labeled cholesterol in fractions with electrophoretic gamma and alpha mobility than E+/+ and E-/-hTgE+/0 plasma. Thus, low-dose expression of apoE in macrophages nearly restored the cholesterol efflux capacity of apoE-deficient plasma through the formation of apoE-containing particles, which efficiently take up cell-derived cholesterol, and through the increase of cholesterol esterification activity. Thus, macrophage-derived apoE may protect against atherosclerosis by increasing cholesterol efflux from arterial wall cells.
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