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Liver receptor homolog 1 controls the expression of the scavenger receptor class B type I
Author(s) -
Schoonjans Kristina,
Annicotte JeanSebastien,
Huby Thierry,
Botrugno Oronza A.,
Fayard Elisabeth,
Ueda Yukihiko,
Chapman John,
Auwerx Johan
Publication year - 2002
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1093/embo-reports/kvf238
Subject(s) - scavenger receptor , liver receptor homolog 1 , nuclear receptor , biology , receptor , liver x receptor , histone , acetylation , reverse cholesterol transport , endocrinology , medicine , microbiology and biotechnology , cholesterol , gene , biochemistry , transcription factor , lipoprotein
The scavenger receptor class B type I (SR‐BI), which mediates selective cellular cholesterol uptake from high‐density lipoproteins (HDLs), plays a key role in reverse cholesterol transport. The orphan nuclear receptor liver receptor homolog 1 (LRH‐1) and SR‐BI are co‐expressed in liver and ovary, suggesting that LRH‐1 might control the expression of SR‐BI in these tissues. LRH‐1 induces human and mouse SR‐BI promoter activity by binding to an LRH‐1 response element in the promoter. Retroviral expression of LRH‐1 robustly induces SR‐BI, an effect associated with histone H3 acetylation on the SR‐BI promoter. The decrease in SR‐BI mRNA levels in livers of LRH‐1 +/− animals provides in vivo evidence that LRH‐1 regulates SR‐BI expression. Our data demonstrate that SR‐BI is an LRH‐1 target gene and underscore the pivotal role of LRH‐1 in reverse cholesterol transport.