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pubmed-article:10722729pubmed:abstractTextCytokines have been implicated in the pathogenesis of inflammatory cholestasis. This is due to transcriptional down-regulation of hepatic transporters including the Na(+)/bile acid cotransporter, ntcp, and the multispecific organic anion exporter, mrp2. We have recently shown that ntcp suppression by lipopolysaccharide in vivo is caused by down-regulation of transactivators including the previously uncharacterized Footprint B-binding protein. Both the ntcp FpB element and the mrp2 promoter contain potential retinoid-response elements. We hypothesized that retinoic acid receptor (RAR) and retinoid X receptor (RXR) heterodimers would activate these two genes and that cytokines that reduce bile flow might do so by suppressing nuclear levels of these transactivators. Retinoid transactivation and interleukin-1beta down-regulation of the ntcp and mrp2 promoters were mapped to RXRalpha:RARalpha-response elements. Gel mobility shift assays demonstrated specific binding of RXRalpha:RARalpha heterodimers to the ntcp and mrp2 retinoid-response elements. The RXRalpha:RARalpha complex was down-regulated by IL-1beta in HepG2 cells. An unexpected finding was that an adjacent CAAT-enhancer-binding protein element was required for maximal transactivation of the ntcp promoter by RXRalpha:RARalpha. Taken together, these studies demonstrate regulation of two hepatobiliary transporter genes by RXRalpha:RARalpha and describe a mechanism which likely contributes to their down-regulation during inflammation.lld:pubmed
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pubmed-article:10722729pubmed:articleTitleInterleukin-1beta suppresses retinoid transactivation of two hepatic transporter genes involved in bile formation.lld:pubmed
pubmed-article:10722729pubmed:affiliationDepartment of Pediatrics, Yale University School of Medicine, New Haven, Connecticut 06520, USA.lld:pubmed
pubmed-article:10722729pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10722729pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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