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Article: Polarized cholesterol and phospholipid efflux in cultured gall-bladder epithelial cells: Evidence for an ABCA1-mediated pathway

TitlePolarized cholesterol and phospholipid efflux in cultured gall-bladder epithelial cells: Evidence for an ABCA1-mediated pathway
Authors
Issue Date2002
PublisherPortland Press Ltd. The Journal's web site is located at http://www.biochemj.org
Citation
Biochemical Journal, 2002, v. 364 n. 2, p. 475-484 How to Cite?
AbstractGall-bladder epithelial cells (GBEC) are exposed to high concentrations of cholesterol in bile. Whereas cholesterol absorption by GBEC is established, the fate of this absorbed cholesterol is not known. The aim of this study was to determine whether ABCA1 (ATP-binding cassette transporter A1) mediates cholesterol efflux in GBEC. Polarized canine GBEC were cultured on porous membrane filters allowing separate access to apical (AP) and basolateral (BL) compartments. After AP loading of cells with model bile and [ 14C]cholesterol, cholesterol efflux was measured. Cholesterol loading together with 8-bromo-cAMP treatment, which increased ABCA1 expression, led to a significant increase in cholesterol efflux with apolipoprotein A-I (apoA-I) as the acceptor. Cholesterol efflux was observed predominantly into the BL compartment. Similar results were found for phospholipid efflux. Confocal immunofluorescence microscopy showed a predominantly BL ABCA1 localization. Interestingly, apoA-I added to either the AP or the BL compartments elicited BL lipid efflux with cAMP treatment. No paracellular or transcellular passage of 125I-apoA-I occurred. Ligands for the nuclear hormone receptors liver X receptor α (LXRα) and retinoid X receptor (RXR) elicited AP and BL cholesterol efflux, suggesting the involvement of both ABCA1- and non-ABCA1-mediated pathways. In summary, BL cholesterol/phospholipid efflux consistent with an ABCA1-mediated mechanism occurs in GBEC. This efflux pathway is stimulated by cAMP and by LXRα/RXR ligands, and in the case of the cAMP pathway appears to involve a role for biliary apoA-I.
Persistent Identifierhttp://hdl.handle.net/10722/175865
ISSN
2015 Impact Factor: 3.562
2015 SCImago Journal Rankings: 2.582
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, Jen_US
dc.contributor.authorShirk, Aen_US
dc.contributor.authorOram, JFen_US
dc.contributor.authorLee, SPen_US
dc.contributor.authorKuver, Ren_US
dc.date.accessioned2012-11-26T09:01:53Z-
dc.date.available2012-11-26T09:01:53Z-
dc.date.issued2002en_US
dc.identifier.citationBiochemical Journal, 2002, v. 364 n. 2, p. 475-484en_US
dc.identifier.issn0264-6021en_US
dc.identifier.urihttp://hdl.handle.net/10722/175865-
dc.description.abstractGall-bladder epithelial cells (GBEC) are exposed to high concentrations of cholesterol in bile. Whereas cholesterol absorption by GBEC is established, the fate of this absorbed cholesterol is not known. The aim of this study was to determine whether ABCA1 (ATP-binding cassette transporter A1) mediates cholesterol efflux in GBEC. Polarized canine GBEC were cultured on porous membrane filters allowing separate access to apical (AP) and basolateral (BL) compartments. After AP loading of cells with model bile and [ 14C]cholesterol, cholesterol efflux was measured. Cholesterol loading together with 8-bromo-cAMP treatment, which increased ABCA1 expression, led to a significant increase in cholesterol efflux with apolipoprotein A-I (apoA-I) as the acceptor. Cholesterol efflux was observed predominantly into the BL compartment. Similar results were found for phospholipid efflux. Confocal immunofluorescence microscopy showed a predominantly BL ABCA1 localization. Interestingly, apoA-I added to either the AP or the BL compartments elicited BL lipid efflux with cAMP treatment. No paracellular or transcellular passage of 125I-apoA-I occurred. Ligands for the nuclear hormone receptors liver X receptor α (LXRα) and retinoid X receptor (RXR) elicited AP and BL cholesterol efflux, suggesting the involvement of both ABCA1- and non-ABCA1-mediated pathways. In summary, BL cholesterol/phospholipid efflux consistent with an ABCA1-mediated mechanism occurs in GBEC. This efflux pathway is stimulated by cAMP and by LXRα/RXR ligands, and in the case of the cAMP pathway appears to involve a role for biliary apoA-I.en_US
dc.languageengen_US
dc.publisherPortland Press Ltd. The Journal's web site is located at http://www.biochemj.orgen_US
dc.relation.ispartofBiochemical Journalen_US
dc.subject.meshAtp-Binding Cassette Transporters - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApolipoprotein A-I - Metabolismen_US
dc.subject.meshBiological Transporten_US
dc.subject.meshCholesterol - Metabolismen_US
dc.subject.meshDna-Binding Proteinsen_US
dc.subject.meshDogsen_US
dc.subject.meshEpithelial Cells - Cytology - Metabolismen_US
dc.subject.meshGallbladder - Cytology - Metabolismen_US
dc.subject.meshLigandsen_US
dc.subject.meshMicroscopy, Fluorescenceen_US
dc.subject.meshOrphan Nuclear Receptorsen_US
dc.subject.meshPhospholipids - Metabolismen_US
dc.subject.meshReceptors, Cytoplasmic And Nuclear - Metabolismen_US
dc.subject.meshReceptors, Retinoic Acid - Metabolismen_US
dc.subject.meshRetinoid X Receptorsen_US
dc.subject.meshTranscription Factors - Metabolismen_US
dc.titlePolarized cholesterol and phospholipid efflux in cultured gall-bladder epithelial cells: Evidence for an ABCA1-mediated pathwayen_US
dc.typeArticleen_US
dc.identifier.emailLee, SP: sumlee@hku.hken_US
dc.identifier.authorityLee, SP=rp01351en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1042/BJ20011493en_US
dc.identifier.pmid12023891-
dc.identifier.scopuseid_2-s2.0-0036606671en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036606671&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume364en_US
dc.identifier.issue2en_US
dc.identifier.spage475en_US
dc.identifier.epage484en_US
dc.identifier.isiWOS:000176180400017-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLee, J=26663282200en_US
dc.identifier.scopusauthoridShirk, A=36449267500en_US
dc.identifier.scopusauthoridOram, JF=7005064740en_US
dc.identifier.scopusauthoridLee, SP=7601417497en_US
dc.identifier.scopusauthoridKuver, R=6701723533en_US

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