Carbon Monoxide Induced PPARγ SUMOylation and UCP2 Block Inflammatory Gene Expression in Macrophages 英文参考文献.docVIP

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Carbon Monoxide Induced PPARγ SUMOylation and UCP2 Block Inflammatory Gene Expression in Macrophages 英文参考文献.doc

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Carbon Monoxide Induced PPARγ SUMOylation and UCP2 Block Inflammatory Gene Expression in Macrophages 英文参考文献

CarbonMonoxideInducedPPARcSUMOylationand UCP2BlockInflammatoryGeneExpressionin Macrophages ArvandHaschemi1.,BeekYokeChin2.,MarkusJeitler1,HaraldEsterbauer1,OswaldWagner1 ,Martin Bilban1.*,LeoEOtterbein2. 1Department ofLaboratoryMedicine,MedicalUniversityofVienna,Vienna,Austria,2Department ofSurgery,BethIsraelDeaconessMedicalCenter,HarvardMedical School,Boston,Massachusetts,UnitedStatesofAmerica Abstract Carbonmonoxide(CO)dampenspro-inflammatoryresponsesinaperoxisomeproliferator-activatedreceptor-c(PPARc )and p38 mitogen-activated protein kinase (MAPK) dependent manner. Previously, we demonstrated that CO inhibits lipopolysaccharide (LPS)-induced expression of the proinflammatory early growth response-1 (Egr-1) transcription factor inmacrophagesviaactivationofPPARc.Here,wefurthercharacterizethemolecularmechanismsbywhichCOmodulates theactivityofPPARcandEgr-1repression.WedemonstratethatCOenhancesSUMOylationofPPARcwhichwefindwas attributedtomitochondrialROSgeneration.EctopicexpressionofaSUMOylation-defectivePPARc-K365Rmutantpartially abolishedCO-mediatedsuppressionofLPS-inducedEgr-1promoteractivity.ExpressionofaPPARc-K77Rmutantdidnot impairtheeffectofCO.InadditiontoPPARcSUMOylation,CO-activatedp38MAPKwasresponsibleforEgr-1repression. BlockingbothCO-inducedPPARcSUMOylationandp38activation,completelyreversedtheeffectsofCOoninflammatory geneexpression.InprimarymacrophagesisolatedformC57/BL6malemice,weidentifymitochondrialROSformationbyCO as the upstream trigger for the observed effects on Egr-1 in part through uncoupling protein 2 (UCP2). Macrophages derivedfrombonemarrowisolatedfromUcp2geneKnock-OutC57/BL6mice(Ucp22/2),producedsignificantlylessROS withCOexposureversuswild-typemacrophages.Moreover,absenceofUCP2resultedinacompletelossofCOmediated Egr-1repression.Collectively,theseresultsindentifyp38activation,PPARc-SUMOylationandROSformationviaUCP2asa cooperativesystembywhichCOimpactstheinflammatoryresponse. Citation:HaschemiA,ChinBY,JeitlerM,EsterbauerH,WagnerO,eta