CD40 Is Essential in the Upregulation of TRAF Proteins and NF-KappaB-Dependent Proinflammatory Gene Expression after Arterial Injury 英文参考文献.docVIP

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CD40 Is Essential in the Upregulation of TRAF Proteins and NF-KappaB-Dependent Proinflammatory Gene Expression after Arterial Injury 英文参考文献.doc

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CD40 Is Essential in the Upregulation of TRAF Proteins and NF-KappaB-Dependent Proinflammatory Gene Expression after Arterial Injury 英文参考文献

CD40IsEssentialintheUpregulationofTRAFProteins andNF-KappaB-DependentProinflammatoryGene ExpressionafterArterialInjury ZifangSong1.,RongJin1.,ShiyongYu1,JoshuaJ.Rivet1,SusanS.Smyth3,AnilNanda1,D.Neil Granger2,GuohongLi1,2* 1Vascular Biology and Stroke Research Laboratory, Department of Neurosurgery, LSU Health Science Center in Shreveport, Shreveport, Louisiana, United States of America,2DepartmentofPhysiology,LSUHealthScienceCenterinShreveport,Shreveport,Louisiana,UnitedStatesofAmerica,3DepartmentofMedicine,Universityof Kentucky,Lexington,Kentucky,UnitedStatesofAmerica Abstract Despiteextensiveinvestigations,restenosis,whichischaracterizedprimarilybyneointimaformation,remainsanunsolved clinicalproblemaftervascularinterventions.ArecentstudyhasshownthatCD40signalingthroughTNFreceptorassociated factor6(TRAF6)playsakeyroleinneointimaformationaftercarotidarteryinjury;however,underlyingmechanismsarenot clearlyelucidated.Becauseneointimaformationmayvarysignificantlydependingonthetypeofinjury,wefirstassessedthe effectofCD40deficiencyonneointimaformationin2injurymodels,carotidarteryligationandfemoralarterydenudation injury. Compared withwild-type mice, CD40deficiency significantly reduced neointima formation andlumen stenosisin twodifferentmodels.Further,weinvestigatedthemechanismbywhichCD40signalingaffectsneointimaformationafter arterial injury. In wild-type mice, the expression levels of CD40, several TRAF proteins, including TRAF1, TRAF2, TRAF3, TRAF5, andTRAF6, as well as total NF-kB p65and phospho-NF-kB p65, in the carotid artery were markedly upregulated within 3–7 days after carotid ligation. Deficiency of CD40 abolished the injury-induced upregulation of TRAFs including TRAF6andNF-kB-p65intheinjuredvesselwall.Further,CD402/2miceshowedasignificantdecreaseintherecruitmentof neutrophils(at3,7d)andmacrophages(at7,21d)intoinjuredartery;thiseffectwasmostlikelyattributedtoinhibitionof NF-kB activation and marked downregulation of NF-kB-related gene expression, including