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• W2125109896 abstract "Serum levels of HDL are inversely correlated with the risk of coronary heart disease. The anti-atherogenic effect of HDL is partially mediated by its major protein constituent apoA-I. In this study, we identify bile acids that are activators of the nuclear receptor farnesoid X receptor (FXR) as negative regulators of human apoA-I expression. Intrahepatocellular accumulation of bile acids, as seen in patients with progressive familial intrahepatic cholestasis and biliary atresia, was associated with diminished apoA-I serum levels. In human apoA-I transgenic mice, treatment with the FXR agonist taurocholic acid strongly decreased serum concentrations and liver mRNA levels of human apoA-I, which was associated with reduced serum HDL levels. Incubation of human primary hepatocytes and hepatoblastoma HepG2 cells with bile acids resulted in a dose-dependent downregulation of apoA-I expression. Promoter mutation analysis and gel-shift experiments in HepG2 cells demonstrated that bile acid-activated FXR decreases human apoA-I promoter activity by a negative FXR response element mapped to the C site. FXR bound this site and repressed transcription in a manner independent of retinoid X receptor. The nonsteroidal synthetic FXR agonist GW4064 likewise decreased apoA-I mRNA levels and promoter activity in HepG2 cells." @default.
• W2125109896 created "2016-06-24" @default.
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• W2125109896 date "2002-04-01" @default.
• W2125109896 modified "2023-10-12" @default.
• W2125109896 title "Bile acid-activated nuclear receptor FXR suppresses apolipoprotein A-I transcription via a negative FXR response element" @default.
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• W2125109896 doi "https://doi.org/10.1172/jci14505" @default.
• W2125109896 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/150929" @default.
• W2125109896 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11927623" @default.
• W2125109896 hasPublicationYear "2002" @default.
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