ArticlePloS one2020
THP-1 macrophage cholesterol efflux is impaired by palmitoleate through Akt activation.
Article in PloS one, 2020. 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.
- Changes to small RNA expression in macrophages in response to very low-density lipoprotein lipid hydrolysis by lipoprotein lipase and NADPH oxidase inhibition.BMC research notes · 2026Article
- Diabetic kidney disease macrophage cholesterol efflux: a revolution from metabolism to immune.Frontiers in endocrinology · 2025Review
- Cholesterol efflux and macrophage polarization in human adipose tissue.Physiological research · 2022Article
- MK2206 attenuates atherosclerosis by inhibiting lipid accumulation, cell migration, proliferation, and inflammation.Acta pharmacologica Sinica · 2022Article
- Emerging Anti-Atherosclerotic Therapies.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Lipoprotein lipase (LPL) is upregulated in atherosclerotic lesions and it may promote the progression of atherosclerosis, but the mechanisms behind this process are not completely understood. We previously showed that the phosphorylation of Akt within THP-1 macrophages is increased in response to the lipid hydrolysis products generated by LPL from total lipoproteins. Notably, the free fatty acid (FFA) component was responsible for this effect. In the present study, we aimed to reveal more detail as to how the FFA component may affect Akt signalling. We show that the phosphorylation of Akt within THP-1 macrophages increases with total FFA concentration and that phosphorylation is elevated up to 18 hours. We further show that specifically the palmitoleate component of the total FFA affects Akt phosphorylation. This is tied with changes to the levels of select molecular species of phosphoinositides. We further show that the total FFA component, and specifically palmitoleate, reduces apolipoprotein A-I-mediated cholesterol efflux, and that the reduction can be reversed in the presence of the Akt inhibitor MK-2206. Overall, our data support a negative role for the FFA component of lipoprotein hydrolysis products generated by LPL, by impairing macrophage cholesterol efflux via Akt activation.
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