ArticlePloS one2014
Acute sterol o-acyltransferase 2 (SOAT2) knockdown rapidly mobilizes hepatic cholesterol for fecal excretion.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Novel molecular mechanisms of immune evasion in hepatocellular carcinoma: NSUN2-mediated increase of SOAT2 RNA methylation.Cancer communications (London, England) · 2025Article
- The Gut Microbiome Affects Atherosclerosis by Regulating Reverse Cholesterol Transport.Journal of cardiovascular translational research · 2024Review
- The TICE Pathway: Mechanisms and Potential Clinical Applications.Current atherosclerosis reports · 2023Review
- Benzophenones-natural metabolites with great Hopes in drug discovery: structures, occurrence, bioactivities, and biosynthesis.RSC advances · 2023Review
- DNA Methylation of Genes Participating in Hepatic Metabolisms and Function in Fetal Calf Liver Is Altered by Maternal Undernutrition during Gestation.International journal of molecular sciences · 2023Article
- Transintestinal cholesterol excretion in health and disease.Current atherosclerosis reports · 2022Review
- Multi-omics analyses of early liver injury reveals cell-type-specific transcriptional and epigenomic shift.BMC genomics · 2021Article
- Simultaneous Determination of Biliary and Intestinal Cholesterol Secretion Reveals That CETP (Cholesteryl Ester Transfer Protein) Alters Elimination Route in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Shunts, channels and lipoprotein endosomal traffic: a new model of cholesterol homeostasis in the hepatocyte.Journal of biomedical research · 2017Article
- Article
- Emerging roles of flavin monooxygenase 3 in cholesterol metabolism and atherosclerosis.Current opinion in lipidology · 2015Review
- A new model of reverse cholesterol transport: enTICEing strategies to stimulate intestinal cholesterol excretion.Trends in pharmacological sciences · 2015Review
- Intestinal nuclear receptors in HDL cholesterol metabolism.Journal of lipid research · 2015Review
- The TMAO-Generating Enzyme Flavin Monooxygenase 3 Is a Central Regulator of Cholesterol Balance.Cell reports · 2015Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
The primary risk factor for atherosclerotic cardiovascular disease is LDL cholesterol, which can be reduced by increasing cholesterol excretion from the body. Fecal cholesterol excretion can be driven by a hepatobiliary as well as a non-biliary pathway known as transintestinal cholesterol efflux (TICE). We previously showed that chronic knockdown of the hepatic cholesterol esterifying enzyme sterol O-acyltransferase 2 (SOAT2) increased fecal cholesterol loss via TICE. To elucidate the initial events that stimulate TICE, C57Bl/6 mice were fed a high cholesterol diet to induce hepatic cholesterol accumulation and were then treated for 1 or 2 weeks with an antisense oligonucleotide targeting SOAT2. Within 2 weeks of hepatic SOAT2 knockdown (SOAT2HKD), the concentration of cholesteryl ester in the liver was reduced by 70% without a reciprocal increase in hepatic free cholesterol. The rapid mobilization of hepatic cholesterol stores resulted in a ∼ 2-fold increase in fecal neutral sterol loss but no change in biliary cholesterol concentration. Acute SOAT2HKD increased plasma cholesterol carried primarily in lipoproteins enriched in apoB and apoE. Collectively, our data suggest that acutely reducing SOAT2 causes hepatic cholesterol to be swiftly mobilized and packaged onto nascent lipoproteins that feed cholesterol into the TICE pathway for fecal excretion.
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