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Article: ABCG1 mediated oxidized LDL-derived oxysterol efflux from macrophages

TitleABCG1 mediated oxidized LDL-derived oxysterol efflux from macrophages
Authors
KeywordsATP binding cassette transporters
Oxidized LDL
Oxysterols
Reverse cholesterol transport
Scavenger receptor class B type I
Issue Date2009
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
Citation
Biochemical And Biophysical Research Communications, 2009, v. 390 n. 4, p. 1349-1354 How to Cite?
Abstract
Objectives: The uptake of oxidized LDL (oxLDL) by macrophages is a key initial event in atherogenesis, and the removal of oxidized lipids from artery wall via reverse cholesterol transport is considered antiatherogenic. The aims of this study were to investigate the pathways mediating the removal of oxysterols from oxLDL-loaded macrophages, and the subsequent uptake of the oxysterols by hepatocytes. Methods: LDL was labeled with [3H]cholesterol, and LDL-[3H]cholesterol was oxidized by copper using a standard method. [3H]oxysterol formation in oxLDL was analyzed by thin layer chromatography. oxLDL-[3H]sterol was incubated with macrophages, allowing the uptake of [3H]sterol by macrophages. [3H]sterol efflux from macrophages mediated by ATP binding cassette transporters (ABCA1, ABCG1), or scavenger receptor class B type I (SR-BI) was measured. The subsequent uptake of the [3H]sterol by hepatocytes was also determined. Results: 7-Ketocholesterol was the major oxysterol formed in oxLDL, and it was significantly higher in oxLDL compared with that in native LDL (naLDL). oxLDL-derived sterol efflux to HDL from macrophages was significantly increased compared with naLDL-derived sterol, and it was mainly mediated by ABCG1, but not by ABCA1 or SR-BI. Moreover, although HDL dose-dependently induced sterol efflux from macrophages, only the exported sterol by ABCG1 pathway was efficiently taken up by hepatocytes. Conclusions: ABCG1 mediates oxysterol efflux from oxLDL-loaded macrophages, and the exported oxysterol by ABCG1 pathway can be selectively taken up by hepatocytes. © 2009 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/125085
ISSN
2013 Impact Factor: 2.281
ISI Accession Number ID
References

 

Author Affiliations
  1. The University of Hong Kong
  2. The First Affiliated Hospital
DC FieldValueLanguage
dc.contributor.authorXu, Men_HK
dc.contributor.authorZhou, Hen_HK
dc.contributor.authorTan, KCBen_HK
dc.contributor.authorGuo, Ren_HK
dc.contributor.authorShiu, SWMen_HK
dc.contributor.authorWong, Yen_HK
dc.date.accessioned2010-10-31T11:10:32Z-
dc.date.available2010-10-31T11:10:32Z-
dc.date.issued2009en_HK
dc.identifier.citationBiochemical And Biophysical Research Communications, 2009, v. 390 n. 4, p. 1349-1354en_HK
dc.identifier.issn0006-291Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/125085-
dc.description.abstractObjectives: The uptake of oxidized LDL (oxLDL) by macrophages is a key initial event in atherogenesis, and the removal of oxidized lipids from artery wall via reverse cholesterol transport is considered antiatherogenic. The aims of this study were to investigate the pathways mediating the removal of oxysterols from oxLDL-loaded macrophages, and the subsequent uptake of the oxysterols by hepatocytes. Methods: LDL was labeled with [3H]cholesterol, and LDL-[3H]cholesterol was oxidized by copper using a standard method. [3H]oxysterol formation in oxLDL was analyzed by thin layer chromatography. oxLDL-[3H]sterol was incubated with macrophages, allowing the uptake of [3H]sterol by macrophages. [3H]sterol efflux from macrophages mediated by ATP binding cassette transporters (ABCA1, ABCG1), or scavenger receptor class B type I (SR-BI) was measured. The subsequent uptake of the [3H]sterol by hepatocytes was also determined. Results: 7-Ketocholesterol was the major oxysterol formed in oxLDL, and it was significantly higher in oxLDL compared with that in native LDL (naLDL). oxLDL-derived sterol efflux to HDL from macrophages was significantly increased compared with naLDL-derived sterol, and it was mainly mediated by ABCG1, but not by ABCA1 or SR-BI. Moreover, although HDL dose-dependently induced sterol efflux from macrophages, only the exported sterol by ABCG1 pathway was efficiently taken up by hepatocytes. Conclusions: ABCG1 mediates oxysterol efflux from oxLDL-loaded macrophages, and the exported oxysterol by ABCG1 pathway can be selectively taken up by hepatocytes. © 2009 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/descriptionen_HK
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_HK
dc.subjectATP binding cassette transportersen_HK
dc.subjectOxidized LDLen_HK
dc.subjectOxysterolsen_HK
dc.subjectReverse cholesterol transporten_HK
dc.subjectScavenger receptor class B type Ien_HK
dc.subject.meshATP-Binding Cassette Transporters - metabolism-
dc.subject.meshCell Line, Tumor-
dc.subject.meshHepatocytes - metabolism-
dc.subject.meshLipoproteins, LDL - metabolism-
dc.subject.meshMacrophages - metabolism-
dc.titleABCG1 mediated oxidized LDL-derived oxysterol efflux from macrophagesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-291X&volume=390&issue=4&spage=1349&epage=1354 &date=2009&atitle=ABCG1+mediated+oxidized+LDL-derived+oxysterol+efflux+from+macrophages-
dc.identifier.emailTan, KCB:kcbtan@hku.hken_HK
dc.identifier.authorityTan, KCB=rp00402en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bbrc.2009.10.152en_HK
dc.identifier.pmid19895785en_HK
dc.identifier.scopuseid_2-s2.0-70450263334en_HK
dc.identifier.hkuros174663en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70450263334&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume390en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1349en_HK
dc.identifier.epage1354en_HK
dc.identifier.isiWOS:000272650800050-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXu, M=35216470200en_HK
dc.identifier.scopusauthoridZhou, H=24077909100en_HK
dc.identifier.scopusauthoridTan, KCB=8082703100en_HK
dc.identifier.scopusauthoridGuo, R=35336647600en_HK
dc.identifier.scopusauthoridShiu, SWM=7005550652en_HK
dc.identifier.scopusauthoridWong, Y=24073787400en_HK

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