Oxidative Stress Impairs the Heat Stress Response and Delays Unfolded Protein Recovery 英文参考文献.docVIP

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Oxidative Stress Impairs the Heat Stress Response and Delays Unfolded Protein Recovery 英文参考文献.doc

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Oxidative Stress Impairs the Heat Stress Response and Delays Unfolded Protein Recovery 英文参考文献

OxidativeStressImpairstheHeatStressResponseand DelaysUnfoldedProteinRecovery MasaakiAdachi1,2*,YaohuaLiu1,3,KyokoFujii2,StuartK.Calderwood4,AkiraNakai5,KohzohImai2, YasuhisaShinomura2 1Division of Molecular Oncology and Molecular Diagnosis, Sapporo Medical University School of Medicine, Sapporo, Japan, 2First Department of Internal Medicine, SapporoMedicalUniversitySchoolofMedicine,Sapporo,Japan,3DepartmentofNeurosurgery,TheFirstClinicalCollegeofHarbinMedicalUniversity,Harbin,People’s RepublicofChina,4DepartmentofRadiationOncologyBethIsraelDeaconessMedicalCenter,HarvardMedicalSchool,Boston,UnitedStatesofAmerica,5Departmentof BiochemistryandMolecularBiology,YamaguchiUniversitySchoolofMedicine,Ube,Japan Abstract Background:Environmentalchanges,airpollutionandozonedepletionareincreasingoxidativestress,andglobalwarming threatenshealthbyheatstress.Wenowfaceahighriskofsimultaneousexposuretoheatandoxidativestress.However, therehavebeenfewstudiesinvestigatingtheircombinedadverseeffectsoncellviability. Principal Findings: Pretreatment of hydrogen peroxide (H2O2) specifically and highly sensitized cells to heat stress, and enhancedlossofmitochondrialmembranepotential.H2O2exposureimpairedtheHSP40/HSP70inductionasheatshock response(HSR)andtheunfoldedproteinrecovery,andenhancedeIF2aphosphorylationand/orXBP1splicing,landmarks of ER stress. These H O -mediated effects mimicked enhanced heat sensitivity in HSF1 knockdown or knockout cells. 2 2 Importantly,thermalpreconditioningblockedH2O2–mediatedinhibitoryeffectsonrefoldingactivityandrescuedHSF1+/+ MEFs,butneitherblockedtheeffectsnorrescuedHSF1-/-MEFs.ThesedatastronglysuggestthatinhibitionofHSRand refoldingactivityiscrucialforH2O2–mediatedenhancedheatsensitivity. Conclusions:H2O2blocksHSRandrefoldingactivityunderheatstress,therebyleadingtoinsufficientqualitycontroland enhancingERstress.Theseuncontrolledstressresponsesmayenhancecelldeath.Ourdatathushighlightoxidativestress asacrucialfactoraffectingheattolerance. Citation: Adachi