Egr-1 Regulates Autophagy in Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease 英文参考文献.docVIP

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Egr-1 Regulates Autophagy in Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease 英文参考文献.doc

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Egr-1 Regulates Autophagy in Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease 英文参考文献

Egr-1RegulatesAutophagyinCigaretteSmoke-Induced ChronicObstructivePulmonaryDisease Zhi-HuaChen1,2.,HongPyoKim1,2.,FrankC.Sciurba1,Seon-JinLee1,2,CarolFeghali-Bostwick1, DonnaB.Stolz3,RajivDhir4,RodneyJ.Landreneau5,MathewJ.Schuchert5,SamuelA.Yousem4 ,Kiichi Nakahira1,2,JosephM.Pilewski1,JanetS.Lee1,YingzeZhang1,StefanW.Ryter1,2,AugustineM.K.Choi2* 1Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America, 2PulmonaryandCriticalCareMedicine,BrighamandWomen’sHospital,HarvardMedicalSchool,Boston,Massachusetts,UnitedStatesofAmerica,3CenterforBiologic Imaging,DepartmentofCellBiologyandPhysiology,SchoolofMedicine,UniversityofPittsburgh,Pittsburgh,Pennsylvania,UnitedStatesofAmerica,4Departmentof Pathology,SchoolofMedicine,UniversityofPittsburgh,Pittsburgh,Pennsylvania,UnitedStatesofAmerica,5DepartmentofSurgery,UniversityofPittsburgh,Pittsburgh, Pennsylvania,UnitedStatesofAmerica Abstract Background: Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by abnormal cellular responses to cigarette smoke, resulting in tissue destruction and airflow limitation. Autophagy is a degradative processinvolvinglysosomalturnoverofcellularcomponents,thoughitsroleinhumandiseasesremainsunclear. MethodologyandPrincipalFindings:IncreasedautophagywasobservedinlungtissuefromCOPDpatients,asindicatedby electronmicroscopicanalysis,aswellasbyincreasedactivationofautophagicproteins(microtubule-associatedprotein-1light chain-3B,LC3B,Atg4,Atg5/12,Atg7).Cigarettesmokeextract(CSE)isanestablishedmodelforstudyingtheeffectsofcigarette smokeexposureinvitro.Inhumanpulmonaryepithelialcells,exposuretoCSEorhistonedeacetylase(HDAC)inhibitorrapidly inducedautophagy.CSEdecreasedHDACactivity,resultinginincreasedbindingofearlygrowthresponse-1(Egr-1)andE2F factorstotheautophagygeneLC3Bpromoter,andincreasedLC3Bexpression.KnockdownofE2F-4orEgr-1inhibitedCSE- inducedLC3Bexpression.Kn