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1、CholesterolPotentiatesβCholesterolPotentiatesβ-AmyloidGenesisinCulturedHumanUmbilicalVeinEndothelialCellsGuozhiHuang1,2,ZhiqinXue3,XiaHu1,LilyedicalSchool,Changsha,China2DepartmentofAnatomyEmbryology,LoudiVocationalandTechnicalCollege,Loudi,China3DepartmentofAnatomy,XinjiangMedicalUniversity,Ur
2、umqi,China4NeuroscienceResearchCenter,ChangshaMedicalUniversity,Changsha,China5DepartmentsofPhysiology,AnatomyandtheCenterforIntegratedResearchinCognitiveandNeuralSciences,SouthernIllinoisUniversityCarbondale,Carbondale,USA6KeyLaboratoryofHunanProvinceinNeurodegenerativeDisorders,Changsha,China
3、Received20April2016;accepted3June2016;published6June2016Copyright©2016byauthorsandScientificResearchPublishingInc.ThisonsAttributionInternationalLicense(CCBY).creativemons.org/licenses/by/4.0/AbstractCerebralAmyloidAngiopathy(CAA)occursmonlyamongtheelderlyandalmostinvariablyinpatientser’sD
4、isease(AD).Theβ-amyloidpeptides(Aβ)areproducedviatheamyloidogenicprocessingofβ-AmyloidPrecursorProtein(APP)byβ-secretase-1(BACE1)andγ-secretase.VascularendothelialcellsarelatelyshoolecularmachineryofAβproduction,ightparticipateinthedevelopmentofCAA.Hypercholesterolemiaisconsideredariskfactorfor
5、AD,aymodulateendothelialAβproduction.InthepresentstudyyloidogeniccapabilityofHumanUmbilicalVeinEndothelialCells(HUVECs)invitroandexploredtheeffectofcholesterolexposureontheiramyloidogenicpotential.Cholesteroltreatmentsat12.5and25mg/dLsignificantlyelevatedAPP,BACE1andAPPβ-CTFproteinlevelsandβ-si
6、teAPPcleavageactivityincelllysates,andAβ40levelsinculturemedium.Hog/dLattenuatedtheviabilityoftheculturedcellsanddiminishedtheiramyloidogeniccapability.Thesefindingssuggestthathighcholesterolexposureisstressfultovascularendothelialcells,andatacertaindosagerangecanpromoteanamyloidogenicresponsei
7、nthesecells.*Correspondingauthor.G.Z.Huangetal.24Keyer’sDisease,Cholesterol,Neurodegeneration,VascularDementia1.IntroductionCerebralamyloidosisisapathologicalconditioncausedbythedepositionoftheβ-amyloidpeptides(Aβ)intheextracellul
