Lecithin: Cholesterol Acyltransferase Expression Has Minimal Effects on Macrophage Reverse Cholesterol Transport In Vivo
Open accessAbstract
Background— Lecithin:cholesterol acyltransferase (LCAT) catalyzes the formation of plasma cholesteryl ester, plays a key role in high-density lipoprotein metabolism, and has been believed to be critical in the process of reverse cholesterol transport (RCT). Methods and Results— The role of LCAT in RCT from macrophages was quantified with a validated assay involving intraperitoneal injection in mice of 3 H-cholesterol–labeled J774 macrophages and monitoring the appearance of tracer in plasma, liver, bile, and feces. Human LCAT overexpression in human apolipoprotein A-I transgenic mice substantially increased plasma high-density lipoprotein cholesterol levels but surprisingly did not increase macrophage RCT. Even in the setting of coexpression of scavenger receptor BI or cholesteryl ester transfer protein, both of which promoted the transfer of LCAT-derived high-density lipoprotein cholesterol ester to the liver, LCAT overexpression still had no effect on RCT. Serum from LCAT-overexpressing mice had reduced ability to promote cholesterol efflux from macrophages ex vivo via ABCA1. To determine the effect of LCAT deficiency on macrophage RCT, LCAT −/− and LCAT +/− mice were compared with wild-type mice. Despite extremely low plasma levels of high-density lipoprotein cholesterol, LCAT-deficient mice had only a 50% reduction in RCT. LCAT +/− mice had normal RCT despite a significant reduction in high-density lipoprotein cholesterol. Serum from LCAT-deficient mice had increased ability to promote ABCA1-mediated cholesterol efflux from macrophages ex vivo. Conclusions— These results demonstrate that LCAT overexpression does not promote an increased rate of macrophage RCT. Although LCAT activity does become rate limiting in the context of complete LCAT deficiency, RCT is reduced by only 50% even in the absence of LCAT. These data suggest that macrophage RCT may not be as dependent on LCAT activity as has previously been believed.
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The risk of atherosclerosis of carriers of mutations in APOA1, ABCA1 or LCAT is not increased or at most slightly increased.
“The risk of atherosclerosis of mutation carriers is not increased or at most slightly increased [35], possibly because HDL can also transport free cholesterol directly to the liver [36].”
From HDL cholesterol: reappraisal of its clinical relevance (2017) · cites this paper as [36]
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- Authors
- Tanigawa, H., Billheimer, J. T., Tohyama, J.-I., Fuki, I. V., Ng, D. S., Rothblat, G. H., & Rader, D. J.
- Affiliations
- St. Michael's Hospital (CA)
- From the Institute for Translational Medicine and Therapeutics and Cardiovascular Institute, University of Pennsylvania School of Medicine, Philadelphia (H.T., J.T.B., J.-i.T., N.F., D.J.R.); Department of Medicine, St Michael’s Hospital, Toronto, Canada (D.S.N.); and Children’s Hospital of Philadelphia, Philadelphia, Pa (G.H.R.).
- ORCID
- Rader, Daniel J.
- Venue
- Circulation
- Published
- 2009-07-14
- Volume
- 120
- Issue
- 2
- Pages
- 160-169
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- PMC
- PMC2796275
- OpenAlex
- W2047218361
- Cited by
- 90
- References
- 31
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 1 · 2023: 3 · 2022: 6 · 2021: 7 · 2020: 3 · 2018: 2 · 2017: 5 · 2016: 3 · 2015: 7 · 2014: 6 · 2013: 7 · 2012: 7
- FWCI
- 11.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01 HL 59407, P01-HL22633, P01HL059407, P01HL022633)
- Topics
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- lecithin:cholesterol acyltransferase, reverse cholesterol transport, macrophages, HDL cholesterol, LCAT deficiency, ABCA1, cholesterol efflux, scavenger receptor BI, cholesteryl ester transfer protein, atherosclerosis
- MeSH terms
- Animals, Biological Transport, Cell Line, Cells, Cultured, Cholesterol, Female, Humans, Injections, Intraperitoneal, Phosphatidylcholine-Sterol O-Acyltransferase, Cholesterol, HDL, Macrophages, Mice, Transgenic, Mice, Knockout, ATP-Binding Cassette Transporters, CD36 Antigens, Mice, Cholesterol Ester Transfer Proteins, ATP Binding Cassette Transporter 1
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