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1、第26卷第2期生物医学工程学杂志Vol.26No.22009年4月JournalofBiomedicalEngineeringApril2009EffectsofShearStressonProteinCActivation,EPCRExpressionAndTMExpressioninEndothelialCells1,23344JunPengHuangqingChenXiaohengLiuRuhengLiXiaohongZheng1(DepartmentofBiologicalSciences,NationalUniversityofSingapore,
2、Singapore117543)2(AcademyofIntegrativeMedicine,FujianTraditionalChineseMedicalCollege,Fuzhou350108,China)3(InstituteofBiomedicalEngineering,WestChinaCenterofMedicalSciences,SichuanUniversity,Chengdu610041,China)4(CollegeofPhysicsandElectronicInformation,DaliUniversity,Dali671003,Ch
3、ina)AbstractTheproteinCanticoagulantpathwayplaysafundamentalroleinthecontrolofcoagulationsystemandinflammatoryresponse.Ithasbeenwellestablishedthatphysiologicallevelsofshearstressinduceendothelialstruc-turalchangeandmodulategeneandproteinexpression.However,theroleofshearstressinpro
4、teinCpathwayre-mainsunknown.Inthepresentstudy,weevaluatedtheeffectofshearstressontheactivationofproteinCaswellasontheexpressionofendothelialproteinCreceptor(EPCR)andthrombomodulin(TM)inhumanumbilicalveinen-dothelialcells(HUVECs)whichwereexposedtoTNF-Aalone,shearstressalone,andTNF-A
5、undershearstress.Wefound:(1)EitherTNF-AorshearstressalonesignificantlyreducedEPCRexpressionandproteinCactivationinHUVECs;andsimultaneousexposureofHUVECstoTNF-AandshearstressresultedinafurtherdecreaseofEPCRexpressionandproteinCactivation(P<0105);(2)SimultaneousexposureofHUVECstoTNF-
6、AandshearstressresultedintheincreaseofsolubleEPCRlevelmoresignificantlythandidtheexposureofHUVECstoeitherTNF-Aorshearstressalone(P<0105);(3)ShearstresssignificantlyincreasedTMexpressiononHUVECs,whereasTNF-AinhibitedTMexpression;shearstresscouldstronglyneutralizeTNF-A.sinhibitiveeff
7、ectonTMexpression.WethereforeconcludethatshearstressmayplayanimportantroleinproteinCpathway,whichmaybefulifilledbyregulatingEPCRexpressionandTMexpressioninendothelialcells.KeywordsShearstressEndothelialproteinCreceptor(EPCR)Thrombomodulin(TM)ProteinCactiva-tion流体剪应力对内皮细胞蛋白C的活化以及蛋白C
8、受体和血栓调节蛋白表达的影响1,2$3344彭军陈槐