NADPH Oxidase 2-Derived Reactive Oxygen Species Mediate FFAs-Induced Dysfunction and Apoptosis of β-Cells via JNK, p38 MAPK and p53 Pathways 英文参考文献.docVIP

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NADPH Oxidase 2-Derived Reactive Oxygen Species Mediate FFAs-Induced Dysfunction and Apoptosis of β-Cells via JNK, p38 MAPK and p53 Pathways 英文参考文献.doc

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NADPH Oxidase 2-Derived Reactive Oxygen Species Mediate FFAs-Induced Dysfunction and Apoptosis of β-Cells via JNK, p38 MAPK and p53 Pathways 英文参考文献

NADPHOxidase2-DerivedReactiveOxygenSpecies MediateFFAs-InducedDysfunctionandApoptosisofb- CellsviaJNK,p38MAPKandp53Pathways HuipingYuan1,2.,XiaoyongZhang3.,XiuqingHuang2,YonggangLu3,WeiqingTang2,YongMan2 ,Shu Wang2,JianzhongXi1*,JianLi2,3* 1DepartmentofBiomedicalEngineering,CollegeofEngineering,PekingUniversity,Beijing,China,2PekingUniversityFifthSchoolofClinicalMedicine,BeijingHospital, Beijing,China,3GraduateSchoolofPekingUnionMedicalCollegeandChineseAcademyofMedicalSciences,Beijing,China Abstract Dysfunctionofb-cellisoneofmajorcharacteristicsinthepathogenesisoftype2diabetes.Thecombinationofobesityand type2diabetes,characterizedas‘diabesity’,isassociatedwithelevatedplasmafreefattyacids(FFAs).Oxidativestresshas beenimplicatedinthepathogenesisofFFA-inducedb-celldysfunction.However,molecularmechanismslinkingbetween reactiveoxygenspecies(ROS)andFFA-inducedb-celldysfunctionandapoptosisarelessclear.Inthepresentstudy,wetest thehypothesisthatNOX2-derivedROSmayplayacriticalroleindysfunctionandapoptosisofb-cellsinducedbyFFA.Our results show that palmitate and oleate (0.5mmol/L, 48h) induced JNK activation and AKT inhibition which resulted in decreased phosphorylation of FOXO1 following nuclear localization and the nucleocytoplasmic translocation of PDX-1, leadingtothereducingofinsulinandultimatelydysfunctionofpancreaticNIT-1cells.Wealsofoundthatpalmitateand oleatestimulatedapoptosisofNIT-1cellsthroughp38MAPK,p53andNF-kBpathway.Moreinterestingly,ourdatasuggest thatsuppressionofNOX2mayrestoreFFA-induceddysfunctionandapoptosisofNIT-1cells.Ourfindingsprovideanew insightoftheNOX2asapotentialnewtherapeutictargetforpreservationofb-cellmassandfunction. Citation:YuanH,ZhangX,HuangX,LuY,TangW,etal.(2010)NADPHOxidase2-DerivedReactiveOxygenSpeciesMediateFFAs-InducedDysfunctionand Apoptosisofb-CellsviaJNK,p38MAPKandp53Pathways.PLoSONE5(12):e15726.doi:10.1371/journal.pone.0015726 Editor:JeffreyM.Gimble,PenningtonBiomedicalResearchCenter,UnitedStatesofAmerica ReceivedSeptember10,2010;Ac