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M106375200v1
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Papers In Press, published online ahead of print October 29, 2001
J. Biol. Chem, 10.1074/jbc.M106375200
Submitted on July 9, 2001
Revised on October 19, 2001
Accepted on October 29, 2001

Sterol regulatory element-binding protein-1c is responsible for cholesterol regulation of ileal bile acid-binding protein gene in vivo. Possible involvement of liver X receptor

Isabelle Zaghini, Jean-François Landrier, Jacques Grober, Stéphane Krief, Stacey A. Jones, Maire-Claude Monnot, Isabelle Lefrère, Michael A. Watson, Jon L. Collins, Hiroshi Fujii, and Philippe Besnard

Laboratory of Nutrition Physiology, ENSBANA, Dijon 21000

Corresponding Author: pbesnard{at}u-bourgogne.fr

Ileal Bile Acid-Binding Protein (I-BABP) is a cytosolic protein that binds bile acid (BA) specifically. In the ileum, it is thought to be implied in their enterohepatic circulation. Since the fecal excretion of BA represents the main physiological way of elimination for cholesterol (CS), the I-BABP gene could have a major function in CS homeostasis. Therefore, the I-BABP gene expression might be controlled by CS. I-BABP mRNA levels were significatively increased when the human enterocyte-like CaCo-2 cells were CS-deprived, and repressed when CS were added to the medium. A highly conserved sterol regularory element-like sequence (SRE) and a putative GC box were found in human I-BABP gene promoter. Different constructs of human I-BABP promoter, cloned upstream of a CAT reporter gene have been used in tranfections studies. CAT activity of the wild type promoter was increased in presence of CS-deprived medium, and conversely, decreased by a CS supplemented medium. The inductive effect of CS depletion was fully abolished when the putative SRE sequence and/or GC box were mutated or deleted. Co-transfections experiments with the mature isoforms of human sterol responsive element-binding proteins (SREBPs) and Sp1 demonstrate that the CS-mediated regulation of I-BABP gene was dependent of these transcriptional factors. Paradoxically, mice subjected to a standard chow supplemented with 2% CS for 14 days exhibited a significant rise in both I-BABP and SREBP1c mRNA levels. We show that in vivo, this upregulation could be explained by a recently described regulatory pathway involving a positive regulation of SREBP1c by Liver-X- Receptor (LXR) following a high CS diet.


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