THEJOURNALOFBIOLOGICALCHEMISTRYVol.279,No.17,IssueofApril23,pp.18091–18097,2004©2004byTheAmericanSocietyforBiochemistryandMolecularBiology,Inc.PrintedinU.S.A.InVivoChromatinRemodelingEventsLeadingtoInflammatoryGeneTranscriptionunderDiabeticConditions*Receivedforpublication,October27,2003,andinrevisedform,February4,2004Published,JBCPapersinPress,February19,2004,DOI10.1074/jbc.M311786200FengMiao,IreneGawGonzalo,LindaLanting,andRamaNatarajan‡FromtheGondaDiabetesCenter,BeckmanResearchInstituteofCityofHope,Duarte,California91010ThetranscriptionfactorNF-␬B(NF-␬B)playsapiv-izingmitochondrialsuperoxideproductioncouldblockthreeotalroleinregulatinginflammatorygeneexpression.Itspathwaysinducedbyhyperglycemicdamage(8).However,theeffectsareoptimizedbyvariouscoactivatorsincludingspecificmolecularmechanismsandnucleareventsinvolvedinDownloadedfromhistoneacetyltransferases(HATs)suchasCBP/p300andthetranscriptionofpathologicalgenesunderdiabeticcondi-p/CAF.Evidenceshowsthathighglucose(HG)condi-tionsarenotfullyresolved.CirculatingmonocytesindiabetictionsmimickingdiabetescanactivatethetranscriptionindividualswouldbecontinuouslyexposedtohyperglycemicofNF-␬B-regulatedinflammatorygenes.However,theconditions.Werecentlyshowedthatinvitrocultureofmono-underlyinginvivotranscriptionandnuclearchromatincytesunderhighglucose(HG)versusnormalglucose(NG)remodelingeventsareunknown.Wethereforecarriedconditionsledtotheactivationofthetranscriptionfactornu-outchromatinimmunoprecipitation(ChIP)assaysinclearfactor␬B(NF-␬B)andsignificantlyincreasedtheexpres-www.jbc.orgmonocytestoidentify1)chromatinfactorsboundtothesionofseveralinflammatorychemokinesandcytokines(9,10).promotersoftumornecrosisfactor-␣(TNF-␣)andre-Thepotentinflammatorycytokine,tumornecrosisfactor-␣latedNF-␬B-regulatedgenesunderHGordiabeticcon-(TNF-␣),chemokine,andmonocytechemoattractantprotein-1ditions,2)specificlysine(Lys(K))residuesonhistoneatFUDANUNIVERSITYSCHOOFPHARMACY,onAugust6,2012H3(HH3)andHH4acetylatedinthis