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The farnesoid X receptor induces very low density lipoprotein receptor gene expression
Author(s) -
Sirvent Audrey,
Claudel Thierry,
Martin Geneviève,
Brozek John,
Kosykh Vladimir,
Darteil Raphaël,
Hum Dean W.,
Fruchart Jean-Charles,
Staels Bart
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.04.026
Subject(s) - farnesoid x receptor , nuclear receptor , chemistry , small heterodimer partner , chenodeoxycholic acid , gene silencing , receptor , lipoprotein , liver x receptor , microbiology and biotechnology , agonist , medicine , endocrinology , bile acid , biology , biochemistry , cholesterol , transcription factor , gene
The farnesoid X receptor (FXR) is a nuclear receptor activated by bile acids (BAs). In response to ligand‐binding, FXR regulates many genes involved in BA, lipid, and lipoprotein metabolism. To identify new FXR target genes, microarray technology was used to profile total RNA extracted from HepG2 cells treated with the natural FXR agonist chenodeoxycholic acid (CDCA). Interestingly, a significant increase of transcript level of the very low density lipoprotein receptor (VLDLR) was observed. Our data, resulting from selective FXR activation, FXR RNA silencing and FXR‐deficient mice, clearly demonstrate that BAs up‐regulate VLDLR transcript levels via a FXR‐dependent mechanism in vitro in human and in vivo in mouse liver cells.