Cited by 250Cholesterol and Lipid MetabolismAtherosclerosis and Cardiovascular DiseasesDrug Transport and Resistance Mechanisms

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Increased ABCA1 activity protects against atherosclerosis

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Singaraja, Roshni R., Fievet, Catherine, Castro, Graciela, James, Erick R., Hennuyer, Nathalie, Clee, Susanne M., Bissada, Nagat, Choy, Jonathan C., Fruchart, Jean-Charles, McManus, Bruce M., Staels, Bart, Hayden, Michael R.·2002·Journal of Clinical Investigation

DOI 10.1172/jci15748PMC PMC151034

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Abstract

The ABC transporter ABCA1 plays a key role in the first steps of the reverse cholesterol transport pathway by mediating lipid efflux from macrophages. Previously, it was demonstrated that human ABCA1 overexpression in vivo in transgenic mice results in a mild elevation of plasma HDL levels and increased efflux of cholesterol from macrophages. In this study, we determined the effect of overexpression of ABCA1 on atherosclerosis development. Human ABCA1 transgenic mice (BAC(+)) were crossed with ApoE(-/-) mice, a strain that spontaneously develop atherosclerotic lesions. BAC(+)ApoE(-/-) mice developed dramatically smaller, less-complex lesions as compared with their ApoE(-/-) counterparts. In addition, there was increased efflux of cholesterol from macrophages isolated from the BAC(+)ApoE(-/-) mice. Although the increase in plasma HDL cholesterol levels was small, HDL particles from BAC(+)ApoE(-/-) mice were significantly better acceptors of cholesterol. Lipid analysis of HDL particles from BAC(+)ApoE(-/-) mice revealed an increase in phospholipid levels, which was correlated significantly with their ability to enhance cholesterol efflux.

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Authors: Singaraja, R. R., Fievet, C., Castro, G., James, E. R., Hennuyer, N., Clee, S. M., Bissada, N., Choy, J. C., Fruchart, J.-C., McManus, B. M., Staels, B., & Hayden, M. R.
Affiliations: University of British Columbia (CA)
Inserm (FR)
Corresponding author: Hayden, Michael R.
ORCID: Singaraja, Roshni R.
James, Erick R.
Hennuyer, Nathalie
Clee, Susanne M.
Choy, Jonathan C.
McManus, Bruce M.
Staels, Bart
Hayden, Michael R.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2002-07-01
Volume: 110
Issue: 1
Pages: 35-42
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci15748
PMC: PMC151034
OpenAlex: W2097061706
Cited by: 250
References: 45
Citations by year: 2024: 2 · 2023: 1 · 2022: 5 · 2021: 8 · 2020: 5 · 2019: 3 · 2018: 3 · 2017: 6 · 2016: 11 · 2015: 9 · 2014: 9 · 2013: 10 · 2012: 8
FWCI: 22.28
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Canadian Institutes of Health Research
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
Keywords: ABCA1, atherosclerosis, reverse cholesterol transport, HDL cholesterol, macrophage cholesterol efflux, ApoE-deficient mice, transgenic mice, phospholipids, HDL particle composition, atherosclerotic plaque
MeSH terms: Animals, Apolipoproteins A, Apolipoproteins E, Arteriosclerosis, Biological Transport, Active, Cholesterol, Humans, Lipoproteins, HDL, Macrophages, Mice, Transgenic, Phospholipids, Tissue Distribution, Apolipoprotein A-I, Mice, Knockout, ATP-Binding Cassette Transporters, Mice, ATP Binding Cassette Transporter 1

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Increased ABCA1 activity protects against atherosclerosis

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