ArticleAmerican journal of physiology. Endocrinology and metabolism2008
25-Hydroxycholesterol-3-sulfate regulates macrophage lipid metabolism via the LXR/SREBP-1 signaling pathway.
Article in American journal of physiology. Endocrinology and metabolism, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- Dynamic regulatory mechanism of cholesterol 25-hydroxylase-mediated antiviral response in RNA virus infections.Frontiers in cellular and infection microbiology · 2026Review
- Oxysterol-mediated modulation of intestinal inflammation: insights into sex differences and GPR183 signaling.Cellular and molecular life sciences : CMLS · 2025Article
- Discovery of a novel regulator, 3β-sulfate-5-cholestenoic acid, of lipid metabolism and inflammation.American journal of physiology. Endocrinology and metabolism · 2025Article
- Bile Acid Signaling in Metabolic and Inflammatory Diseases and Drug Development.Pharmacological reviews · 2024Review
- Larsucosterol: endogenous epigenetic regulator for treating chronic and acute liver diseases.American journal of physiology. Endocrinology and metabolism · 2024Review
- Cholestenoic acid as endogenous epigenetic regulator decreases hepatocyte lipid accumulation in vitro and in vivo.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Review
- Article
- Review
- Studies in the antiviral molecular mechanisms of 25-hydroxycholesterol: Disturbing cholesterol homeostasis and post-translational modification of proteins.European journal of pharmacology · 2022Review
- Article
- Cholesterol Metabolites 25-Hydroxycholesterol and 25-Hydroxycholesterol 3-Sulfate Are Potent Paired Regulators: From Discovery to Clinical Usage.Metabolites · 2020Review
- A chalcone derivative, 1m-6, exhibits atheroprotective effects by increasing cholesterol efflux and reducing inflammation-induced endothelial dysfunction.British journal of pharmacology · 2020Article
- DNA Methylation in Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2020Review
- High Glucose Induces Lipid Accumulation via 25-Hydroxycholesterol DNA-CpG Methylation.iScience · 2020Article
- The marine-derived furanone reduces intracellular lipid accumulation in vitro by targeting LXRα and PPARα.Journal of cellular and molecular medicine · 2020Article
- 6-Ketocholestanol suppresses lipid accumulation by decreasing FASN gene expression through SREBP-dependent regulation in HepG2 cells.Cytotechnology · 2020Article
- Article
- Orally administration ofFood science and biotechnology · 2019Article
- Activation of liver X receptor plays a central role in antiviral actions of 25-hydroxycholesterol.Journal of lipid research · 2018Article
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Authors and funding
8 authors.
Funding
Abstract
The oxysterol receptor LXR is a key transcriptional regulator of lipid metabolism. LXR increases expression of SREBP-1, which in turn regulates at least 32 genes involved in lipid synthesis and transport. We recently identified 25-hydroxycholesterol-3-sulfate (25HC3S) as an important regulatory molecule in the liver. We have now studied the effects of 25HC3S and its precursor, 25-hydroxycholesterol (25HC), on lipid metabolism as mediated by the LXR/SREBP-1 signaling in macrophages. Addition of 25HC3S to human THP-1-derived macrophages markedly decreased nuclear LXR protein levels. 25HC3S administration was followed by dose- and time-dependent decreases in SREBP-1 mature protein and mRNA levels. 25HC3S decreased the expression of SREBP-1-responsive genes, acetyl-CoA carboxylase-1, and fatty acid synthase (FAS) as well as HMGR and LDLR, which are key proteins involved in lipid metabolism. Subsequently, 25HC3S decreased intracellular lipids and increased cell proliferation. In contrast to 25HC3S, 25HC acted as an LXR ligand, increasing ABCA1, ABCG1, SREBP-1, and FAS mRNA levels. In the presence of 25HC3S, 25HC, and LXR agonist T0901317, stimulation of LXR targeting gene expression was repressed. We conclude that 25HC3S acts in macrophages as a cholesterol satiety signal, downregulating cholesterol and fatty acid synthetic pathways via inhibition of LXR/SREBP signaling. A possible role of oxysterol sulfation is proposed.
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