ArticleThe Journal of steroid biochemistry and molecular biology2012
Cholesterol metabolite, 5-cholesten-3β-25-diol-3-sulfate, promotes hepatic proliferation in mice.
Article in The Journal of steroid biochemistry and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Discovery of a novel regulator, 3β-sulfate-5-cholestenoic acid, of lipid metabolism and inflammation.American journal of physiology. Endocrinology and metabolism · 2025Article
- Oxysterol sulfates in fluids, cells and tissues: how much do we know about their clinical significance, biological relevance and biophysical implications?Essays in biochemistry · 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
- Article
- Cholesterol Metabolites 25-Hydroxycholesterol and 25-Hydroxycholesterol 3-Sulfate Are Potent Paired Regulators: From Discovery to Clinical Usage.Metabolites · 2020Review
- Disrupting LXRα phosphorylation promotes FoxM1 expression and modulates atherosclerosis by inducing macrophage proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Synthesis and Application of Injectable Bioorthogonal Dendrimer Hydrogels for Local Drug Delivery.ACS biomaterials science & engineering · 2017Article
- Oxysterol binding protein-related protein 8 mediates the cytotoxicity of 25-hydroxycholesterol.Journal of lipid research · 2016Article
- Liver X receptor α is essential for the capillarization of liver sinusoidal endothelial cells in liver injury.Scientific reports · 2016Article
- Sulfation of 25-hydroxycholesterol regulates lipid metabolism, inflammatory responses, and cell proliferation.American journal of physiology. Endocrinology and metabolism · 2014Review
- Identification of novel regulatory cholesterol metabolite, 5-cholesten, 3β,25-diol, disulfate.PloS one · 2014Article
- Hydroxysteroid sulfotransferase SULT2B1b promotes hepatocellular carcinoma cells proliferation in vitro and in vivo.PloS one · 2013Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
unlabelledOxysterols are well known as physiological ligands of liver X receptors (LXRs). Oxysterols, 25-hydroxycholesterol (25HC) and 27-hydroxycholesterol as endogenous ligands of LXRs, suppress cell proliferation via LXRs signaling pathway. Recent reports have shown that sulfated oxysterol, 5-cholesten-3β-25-diol-3-sulfate (25HC3S) as LXRs antagonist, plays an opposite direction to oxysterols in lipid biosynthesis. The present report was to explore the effect and mechanism of 25HC3S on hepatic proliferation in vivo. Following administration, 25HC3S had a 48 h half life in the circulation and widely distributed in mouse tissues. Profiler™ PCR array and RTqPCR analysis showed that either exogenous or endogenous 25HC3S generated by overexpression of oxysterol sulfotransferase (SULT2B1b) plus administration of 25HC significantly up-regulated the proliferation gene expression of Wt1, Pcna, cMyc, cyclin A, FoxM1b, and CDC25b in a dose-dependent manner in liver while substantially down-regulating the expression of cell cycle arrest gene Chek2 and apoptotic gene Apaf1. Either exogenous or endogenous administration of 25HC3S significantly induced hepatic DNA replication as measured by immunostaining of the PCNA labeling index and was associated with reduction in expression of LXR response genes, such as ABCA1 and SREBP-1c. Synthetic LXR agonist T0901317 effectively blocked 25HC3S-induced hepatic proliferation.
conclusions25HC3S may be a potent regulator of hepatocyte proliferation and oxysterol sulfation may represent a novel regulatory pathway in liver proliferation via inactivating LXR signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.