Akt Regulates IL-10 Mediated Suppression of TNFα-Induced Cardiomyocyte Apoptosis by Upregulating Stat3 Phosphorylation 英文参考文献.docVIP

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Akt Regulates IL-10 Mediated Suppression of TNFα-Induced Cardiomyocyte Apoptosis by Upregulating Stat3 Phosphorylation 英文参考文献.doc

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Akt Regulates IL-10 Mediated Suppression of TNFα-Induced Cardiomyocyte Apoptosis by Upregulating Stat3 Phosphorylation 英文参考文献

AktRegulatesIL-10MediatedSuppressionofTNFa- InducedCardiomyocyteApoptosisbyUpregulatingStat3 Phosphorylation SanjivDhingra,AshimK.Bagchi,AnaL.Ludke,AnitaK.Sharma,PawanK.Singal* Department ofPhysiology, FacultyofMedicine,Institute ofCardiovascular Sciences, St.BonifaceGeneral Hospital ResearchCenter, University of Manitoba, Winnipeg, Canada Abstract Background:WehavealreadyreportedthatTNF-aincreasescardiomyocyteapoptosisandIL-10treatmentpreventedthese effectsofTNF-a.PresentstudyinvestigatestheroleofAktandJak/StatpathwayintheIL-10modulationofTNF-ainduced cardiomyocyteapoptosis. Methodology/Principalfindings:CardiomyocytesisolatedfromadultSpragueDawleyratswereexposedtoTNF-a(10ng/ ml),IL-10(10ng/ml)andTNF-a+IL-10(ratio1)for4h.ExposuretoTNF-aresultedinanincreaseincardiomyocyteapoptosis asmeasuredbyflowcytometryandTUNELassay.IL-10byitselfhadnoeffect,butitpreventedTNF-ainducedapoptosis.IL- 10treatmentincreasedAktlevelswithincardiomyocytesandthischangewasassociatedwithanincreaseinJak1andStat3 phosphorylation.Pre-exposureofcellstoAktinhibitorpreventedIL-10inducedStat3phosphorylation.Furthermore,inthe presenceofAktorStat3inhibitor,IL-10treatmentwasunabletoblockTNF-ainducedcardiomyocyteapoptosis. Conclusion:ItissuggestedthatIL-10modulationofTNF-ainducedcardiomyocyteapoptosisismediatedbyAktviaStat3 activation. Citation:DhingraS,BagchiAK,LudkeAL,SharmaAK,SingalPK(2011)AktRegulatesIL-10MediatedSuppressionofTNFa-InducedCardiomyocyteApoptosisby UpregulatingStat3Phosphorylation.PLoSONE6(9):e25009.doi:10.1371/journal.pone.0025009 Editor:Malu′ G.Tansey,EmoryUniversity,UnitedStatesofAmerica ReceivedJuly14,2011;AcceptedAugust22,2011;PublishedSeptember20,2011 Copyright: ? 2011 Dhingra et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding:ThestudywassupportedbyanoperatinggrantfromCanadianInstituteofHealthR