Apo A1 Mimetic Rescues the Diabetic Phenotype of HO-2 Knockout Mice via an Increase in HO-1 Adiponectin and LKBI Signaling Pathway英文文献资料.docVIP

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Apo A1 Mimetic Rescues the Diabetic Phenotype of HO-2 Knockout Mice via an Increase in HO-1 Adiponectin and LKBI Signaling Pathway英文文献资料.doc

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Apo A1 Mimetic Rescues the Diabetic Phenotype of HO-2 Knockout Mice via an Increase in HO-1 Adiponectin and LKBI Signaling Pathway英文文献资料

HindawiPublishingCorporation InternationalJournalofHypertension Volume2012,ArticleID628147,8pages doi:10.1155/2012/628147 ResearchArticle ApoA1MimeticRescuestheDiabeticPhenotypeofHO-2 KnockoutMiceviaanIncreaseinHO-1AdiponectinandLKBI SignalingPathway JianCao, NitinPuri, KomalSodhi, LarsBellner, 1 2 2 3 2 NaderG.Abraham, andAttallahKappas 4 1 2 3 4 DepartmentofGeriatricCardiology,ChinesePLAGeneralHospital,Beijing100853,China DepartmentofPhysiologyandPharmacology,CollegeofMedicine,UniversityofToledo,Toledo,OH43614,USA DepartmentofPharmacology,NewYorkMedicalCollege,Valhalla,NY10595,USA TheRockefellerUniversity,NewYork,NY10065,USA CorrespondenceshouldbeaddressedtoJianCao,calvin301@163.com Received11October2011;Revised5December2011;Accepted6December2011 AcademicEditor:DavidE.Stec Copyright?2012JianCaoetal.ThisisanopenaccessarticledistributedundertheCreativeCommonsAttributionLicense,which permitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperlycited. Insulinresistance,withadiposetissuedysfunction,isoneofthehallmarksofmetabolicsyndrome.Wehavereportedametabolic syndrome-likephenotypeinhemeoxygenase(HO)-2knockoutmice,whichpresentedwithconcurrentHO-1de?ciencyandwere amenabletorescuebyanEETanalog.ApoA-Imimeticpeptides,suchasL-4F,havebeenshowntoinduceHO-1expressionand decreaseoxidativestressandadiposity.Inthisstudyweaimedtocharacterizealleviatorye?ectsofHO-1induction(ifany)on metabolicimbalanceobservedinHO-2KOmice.Inthisregard,HO-2(?/?)micewereinjectedwith2mg/kg/dayL-4F,orvehicle, i.p.,for6weeks.Asbefore,comparedtoWTanimals,theHO-2nullmicewereobese,displayedinsulinresistance,andhadelevated bloodpressure.Thesechangeswereaccompaniedbyenhancedtissue(hepatic)oxidativestressalongwithattenuationofHO-1 expressionandactivityandreducedadiponectin,pAMPK,andLKB1expression.TreatmentwithL-4FrestoredHO-1expression andactivityandincreasedadiponectin,LKB1,andpAMPKintheHO-2(?/?)mice.Thesealterationsresultedinadecreaseinblood p