ArticleFrontiers in pharmacology2017
The Dietary Constituent Falcarindiol Promotes Cholesterol Efflux from THP-1 Macrophages by Increasing ABCA1 Gene Transcription and Protein Stability.
Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Divergent fatty acid desaturase 2 is essential for falcarindiol biosynthesis in carrot.Plant communications · 2025Article
- Role ofCurrent medicinal chemistry · 2025Review
- Article
- 24-Hydroxycholesterol Moderates the Effects of Amyloid-β on Expression of HMG-CoA Reductase and ABCA1 Proteins in Mouse Astrocytes.Advanced biomedical research · 2023Article
- Falcarindiol Purified From Carrots Leads to Elevated Levels of Lipid Droplets and Upregulation of Peroxisome Proliferator-Activated Receptor-γ Gene Expression in Cellular Models.Frontiers in pharmacology · 2020Article
- The Forty-Sixth Euro Congress on Drug Synthesis and Analysis: SnapshotMolecules (Basel, Switzerland) · 2017Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
We report increased cholesterol efflux from macrophages in the presence of falcarindiol, an important dietary constituent present in commonly used vegetables and medicinal plants. Falcarindiol (3-20 μM) increased cholesterol efflux from THP-1-derived macrophages. Western blot analysis showed an increased protein level of ABCA1 upon falcarindiol exposure. Quantitative real-time PCR revealed that also ABCA1 mRNA level rise with falcarindiol (10 μM) treatment. The effect of falcarindiol on ABCA1 protein as well as mRNA level were counteracted by co-treatment with BADGE, an antagonist of PPARγ. Furthermore, falcarindiol significantly inhibited ABCA1 protein degradation in the presence of cycloheximide. This post-translational regulation of ABCA1 by falcarindiol occurs most likely by inhibition of lysosomal cathepsins, resulting in decreased proteolysis and extended protein half-life of ABCA1. Taken together, falcarindiol increases ABCA1 protein level by two complementary mechanisms, i.e., promoting ABCA1 gene expression and inhibiting ABCA1 protein degradation, which lead to enhanced cholesterol efflux.
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Registered trials
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