HCV Causes Chronic Endoplasmic Reticulum Stress Leading to Adaptation and Interference with the Unfolded Protein Response 英文参考文献.docVIP

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HCV Causes Chronic Endoplasmic Reticulum Stress Leading to Adaptation and Interference with the Unfolded Protein Response 英文参考文献.doc

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HCV Causes Chronic Endoplasmic Reticulum Stress Leading to Adaptation and Interference with the Unfolded Protein Response 英文参考文献

HCVCausesChronicEndoplasmicReticulumStress LeadingtoAdaptationandInterferencewiththe UnfoldedProteinResponse EmmanuelleMerquiol1,DotanUzi1,TobiasMueller3,DanielGoldenberg4,YaakovNahmias5,RamnikJ. Xavier6,BoazTirosh2.,OrenShibolet7*. 1Liver Unit, Division of Medicine, Hadassah-Hebrew University Medical Center, Jerusalem, Israel, 2Institute for Drug Research, School of Pharmacology, Faculty of Medicine,Jerusalem,Israel, 3Medizinische KlinikM. S.Hepatologieund Gastroenterologie, Charite′ -Universita¨tsmedizin Berlin, CVK,Berlin,Germany, 4Goldyne Savad InstituteofGeneTherapy,Hadassah-HebrewUniversityMedicalCenter,Jerusalem,Israel,5CenterforBioengineering,RachelandSelimBeninSchoolofComputerScience andEngineering,SilbermanInstituteofLifeSciences,TheHebrewUniversityofJerusalem,Jerusalem,Israel,6GastroenterologyUnit,CenterfortheStudyofInflammatory BowelDisease,andCenterforComputationalandIntegrativeBiology,MassachusettsGeneralHospitalandHarvardMedicalSchool,Boston,Massachusetts,UnitedStates ofAmerica,7LiverUnit,DepartmentofGastroenterologyandLiverDisease,Tel-AvivSouraskyMedical-Center,Tel-Aviv,Israel Abstract Background:Theendoplasmicreticulum(ER)isthecellularsiteforproteinfolding.ERstressoccurswhenproteinfolding capacityisexceeded.Thisstressinducesacyto-protectivesignalingcascadestermedtheunfoldedproteinresponse(UPR) aimed at restoring homeostasis. While acute ER stress is lethal, chronic sub-lethal ER stress causes cells to adapt by attenuationofUPRactivation.HepatitisCvirus(HCV),amajorhumanpathogen,wasshowntocauseERstress,howeveritis unclear whether HCV induces chronic ER stress, and if so whether adaptation mechanisms are initiated. We wanted to characterize the kinetics of HCV-induced ER stress during infection and assess adaptation mechanisms and their significance. MethodsandFindings:TheHuH7.5.1cellularsystemandHCV-transgenic(HCV-Tg)micewereusedtocharacterizeHCV- inducedERstress/UPRpathwayactivationandadaptation.HCVinducedawaveofacuteERstresspeaking2–5dayspost- i