O-GlcNAc Modification of NFκB p65 Inhibits TNF-α-Induced Inflammatory Mediator Expression in Rat Aortic Smooth Muscle Cells 英文参考文献.docVIP

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O-GlcNAc Modification of NFκB p65 Inhibits TNF-α-Induced Inflammatory Mediator Expression in Rat Aortic Smooth Muscle Cells 英文参考文献.doc

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O-GlcNAc Modification of NFκB p65 Inhibits TNF-α-Induced Inflammatory Mediator Expression in Rat Aortic Smooth Muscle Cells 英文参考文献

O-GlcNAcModificationofNFkBp65Inhibits TNF-a-InducedInflammatoryMediatorExpression inRatAorticSmoothMuscleCells DongqiXing1*.,KaizhengGong1,4.,WenguangFeng1,SusanE.Nozell2,Yiu-FaiChen1,JohnC. Chatham3,SuzanneOparil1 1VascularBiologyandHypertensionProgram,DivisionofCardiovascularDisease,DepartmentofMedicine,UniversityofAlabamaatBirmingham,Birmingham,Alabama, UnitedStatesofAmerica,2DepartmentofCellBiology,UniversityofAlabamaatBirmingham,Birmingham,Alabama,UnitedStatesofAmerica,3DivisionofMolecular andCellularPathology,DepartmentofPathology,UniversityofAlabamaatBirmingham,Birmingham,Alabama,UnitedStatesofAmerica, 4DivisionofCardiovascular Disease,DepartmentofMedicine,YangzhouUniversity,Yangzhou,Jiangsu,China Abstract Background: We have shown that glucosamine (GlcN) or O-(2-acetamido-2-deoxy-D-glucopyranosylidene)amino-N- phenylcarbamate (PUGNAc) treatment augments O-linked-N-acetylglucosamine (O-GlcNAc) protein modification and attenuatesinflammatorymediatorexpression,leukocyteinfiltrationandneointimaformationinballooninjuredratcarotid arteriesandhaveidentifiedthearterialsmoothmusclecell(SMC)asthetargetcellintheinjuryresponse.NFk Bsignaling has been shown to mediate the expression of inflammatory genes and neointima formation in injured arteries. Phosphorylation of the p65 subunit of NFkB is required for the transcriptional activation of NFkB. This study tested the hypothesis that GlcN or PUGNAc treatment protects vascular SMCs against tumor necrosis factor (TNF)-a induced inflammatory stress by enhancing O-GlcNAcylation and inhibiting TNF-a induced phosphorylation of NFkB p65, thus inhibitingNFk Bsignaling. Methodology/Principal Findings: Quiescent rat aortic SMCs were pretreated with GlcN (5mM), PUGNAc (1024M) or vehicle and then stimulated with TNF-a (10ng/ml). Both treatments inhibited TNF-a-induced expression of chemokines [cytokine-induced neutrophil chemoattractant (CINC)-2b and monocyte chemotactic protein (MCP)-1] and adhesion molecules[vascularce