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Cited by 279

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Bile acid-activated nuclear receptor FXR suppresses apolipoprotein A-I transcription via a negative FXR response element

Claudel, Thierry, Sturm, Ekkehard, Duez, Hélène, Torra, Inés Pineda, Sirvent, Audrey, Kosykh, Vladimir, Fruchart, Jean-Charles, Dallongeville, Jean, Hum, Dean W., Kuipers, Folkert, Staels, Bart·2002·Journal of Clinical Investigation
DOI 10.1172/jci0214505
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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.

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Cited by

Metadata

Authors
Claudel, T., Sturm, E., Duez, H., Torra, I. P., Sirvent, A., Kosykh, V., Fruchart, J.-C., Dallongeville, J., Hum, D. W., Kuipers, F., & Staels, B.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
2002-04-01
Volume
109
Issue
7
Pages
961-971
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci0214505
OpenAlex
W4249387963
Cited by
279
References
2
FWCI
17.24
Type
journal article
Language
en
Open access
closed

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