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Monocyte/macrophage expression of ABCA1 has minimal contribution to plasma HDL levels
Mehrdad Haghpassand, … , Omar L. Francone, Robert J. Aiello
Mehrdad Haghpassand, … , Omar L. Francone, Robert J. Aiello
Published November 1, 2001
Citation Information: J Clin Invest. 2001;108(9):1315-1320. https://doi.org/10.1172/JCI12810.
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Article

Monocyte/macrophage expression of ABCA1 has minimal contribution to plasma HDL levels

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Abstract

Excess accumulation of cholesterol in macrophages results in foam cell production and lesion development. Recent studies have demonstrated that ATP-binding cassette protein A1 (ABCA1) is highly regulated in macrophages and mediates the efflux of cholesterol and phospholipids to apolipoproteins, a process necessary for HDL formation. The goal of this study was to determine the contribution of monocyte/macrophage ABCA1 to HDL formation in vivo. We generated mice expressing ABCA1 in macrophages and mice with selected inactivation of ABCA1 in macrophages by bone marrow transplantation in ABCA1-deficient (ABC1–/–) and wild-type (WT) mice. At all times, the level of HDL in ABC1–/– recipient mice remained low relative to WT recipient mice irrespective of the genotype of the donor macrophage ABCA1 or high-fat feeding. Expression of WT macrophage ABCA1 in ABC1–/– mice resulted in a small but significant increase in apoA-I levels starting 2 weeks after transplantation. No further increase in apoAI was observed up to 14 weeks after transplantation. The increase in apoAI was accompanied by a small but significant increase in HDL cholesterol 6 weeks after transplantation. The HDL formed as a consequence of the expression of WT macrophage ABCA1 migrated to the alpha position in a two-dimensional gel electrophoresis. These results demonstrate that monocyte/macrophage ABCA1 contributes to HDL formation; however, the contribution to the overall plasma HDL levels is minimal.

Authors

Mehrdad Haghpassand, Patricia-Ann K. Bourassa, Omar L. Francone, Robert J. Aiello

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Usage data is cumulative from May 2024 through May 2025.

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