ArticleJournal of atherosclerosis and thrombosis2019
Loss of ACAT1 Attenuates Atherosclerosis Aggravated by Loss of NCEH1 in Bone Marrow-Derived Cells.
Article in Journal of atherosclerosis and thrombosis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- From Storage to Signaling: Lipid Droplet Lipolysis in Cholesterol Mobilization and Foam Cell Remodeling.Current atherosclerosis reports · 2026Review
- Therapeutic Potential of Bioactive Compounds from Traditional Chinese Medicine in Modulating Macrophage Cholesterol Metabolism for Atherosclerosis Treatment.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Targeting Regulation of Macrophage to Treat Metabolic Disease: Role of Phytochemicals.Cell proliferation · 2025Review
- ISG15 Is a Novel Regulator of Lipid Metabolism duringMicrobiology spectrum · 2022Article
- MyeloidThe Journal of biological chemistry · 2019Article
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Authors and funding
12 authors.
Funding
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Abstract
aimAcyl-CoA cholesterol acyltransferase 1 (ACAT1) esterifies free cholesterol to cholesteryl esters (CE), which are subsequently hydrolyzed by neutral cholesterol ester hydrolase 1 (NCEH1). The elimination of ACAT1 in vitro reduces the amounts of CE accumulated in Nceh1-deficient macrophages. The present study aimed at examining whether the loss of ACAT1 attenuates atherosclerosis which is aggravated by the loss of NCEH1 in vivo.
methodsLow density lipoprotein receptor (Ldlr)-deficient mice were transplanted with bone marrow from wild-type mice and mice lacking ACAT1, NCEH1, or both. The four types of mice were fed a high-cholesterol diet and, then, were examined for atherosclerosis.
resultsThe cross-sectional lesion size of the recipients of Nceh1-deficient bone marrow was 1.6-fold larger than that of the wild-type bone marrow. The lesions of the recipients of Nceh1-deficient bone marrow were enriched with MOMA2-positive macrophages compared with the lesions of the recipients of the wild-type bone marrow. The size and the macrophage content of the lesions of the recipients of bone marrow lacking both ACAT1 and NCEH1 were significantly smaller than the recipients of the Nceh1-deficient bone marrow, indicating that the loss of ACAT1 decreases the excess CE in the Nceh1-deficient lesions. The collagen-rich and/or mucin-rich areas and en face lesion size were enlarged in the recipients of the Acat1
conclusionThe loss of ACAT1 in bone marrow-derived cells attenuates atherosclerosis, which is aggravated by the loss of NCEH1, corroborating the in vitro functions of ACAT1 (formation of CE) and NCEH1 (hydrolysis of CE).
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