Acute-Phase-HDL Remodeling by Heparan Sulfate Generates a Novel Lipoprotein with Exceptional Cholesterol Efflux Activity from Macrophages 英文参考文献.docVIP
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Acute-Phase-HDL Remodeling by Heparan Sulfate Generates a Novel Lipoprotein with Exceptional Cholesterol Efflux Activity from Macrophages 英文参考文献
Acute-Phase-HDLRemodelingbyHeparanSulfate
GeneratesaNovelLipoproteinwithExceptional
CholesterolEffluxActivityfromMacrophages
Shui-PangTam1,RobertKisilevsky1,2,JohnB.Ancsin1*
1DepartmentofPathologyandMolecularMedicine,Queen’sUniversity,TheSylandMollyAppsResearchCenter,KingstonGeneralHospital,Kingston,Ontario,Canada,
2DepartmentofBiochemistry,Queen’sUniversity,TheSylandMollyAppsResearchCenter,KingstonGeneralHospital,Kingston,Ontario,Canada
Abstract
During episodes of acute-inflammation high-density lipoproteins (HDL), the carrier of so-called good cholesterol,
experiences a major change in apolipoprotein composition and becomes acute-phase HDL (AP-HDL). This altered, but
physiologicallyimportant,HDLhasanincreasedbindingaffinityformacrophagesthatisdependentoncellsurfaceheparan
sulfate(HS).WhileexploringthepropertiesofAP-HDL:HSinteractionswediscoveredthatHScausedsignificantremodeling
of AP-HDL. The physical nature of this change in structure and its potential importance for cholesterol efflux from
cholesterol-loadedmacrophageswasthereforeinvestigated.Inthepresenceofheparin,orHS,AP-HDLsolutionsatpH5.2
becameturbid withinminutes. Analysis by centrifugation andgelelectrophoresis indicated thatAP-HDLwas remodeled
generating novel lipid poor particles composed only of apolipoprotein AI, which we designate b2. This remodeling is
dependent on pH, glycosaminoglycan type, is promoted by Ca2+ and is independent of protease or lipase activity.
Compared to HDL and AP-HDL, remodeled AP-HDL (S-HDL-SAA), containing b2 particles, demonstrated a 3-fold greater
cholesteroleffluxactivityfromcholesterol-loadedmacrophage.BecausetheidentifiedconditionscausingthischangeinAP-
HDLstructureandfunctioncanexistphysiologicallyatthesurfaceofthemacrophage,orinitsendosomes,wepostulate
that AP-HDL contains latent functionalities that become apparent and active when it associates with macrophage cell
surface/endosomalHS.Inthiswayinitialstepsinthereversecholesteroltransportpathwayarefocusedatsitesofin
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