Activation of JNK Signaling Mediates Amyloid-？-Dependent Cell Death 英文参考文献.docVIP

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Activation of JNK Signaling Mediates Amyloid-？-Dependent Cell Death 英文参考文献.doc

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Activation of JNK Signaling Mediates Amyloid-？-Dependent Cell Death 英文参考文献

ActivationofJNKSignalingMediatesAmyloid-?- DependentCellDeath MeghanaTare1.,RohanM.Modi2.,JaisonJ.Nainaparampil2.,OorvashiRoyPuli1,ShimpiBedi1, PedroFernandez-Funez4,MadhuriKango-Singh1,2,3*,AmitSingh1,2,3 * 1Department of Biology, University of Dayton, Dayton, Ohio, United States of America, 2Premedical Program, University of Dayton, Dayton, Ohio, United States of America,3CenterforTissueRegenerationandEngineeringatDayton(TREND),UniversityofDayton,Dayton,Ohio,UnitedStatesofAmerica,4DepartmentsofNeurology andNeuroscience,McKnightBrainInstitute,UniversityofFlorida,Gainesville,Florida,UnitedStatesofAmerica Abstract Background: Alzheimer’s disease (AD) is an age related progressive neurodegenerative disorder. One of the reasons for Alzheimer’s neuropathology is the generation of large aggregates of A?42 that aretoxic in nature andinduce oxidative stress, aberrant signaling and many other cellular alterations that trigger neuronal cell death. However, the exact mechanismsleadingtocelldeatharenotclearlyunderstood. Methodology/Principal Findings: We employed a Drosophila eye model of AD to study how A?42 causes cell death. Misexpressionofhigherlevels ofA?42inthedifferentiatingphotoreceptorsofflyretinarapidlyinducedaberrant cellular phenotypesandcelldeath.Wefoundthatblockingcaspase-dependentcelldeathinitiallyblockedcelldeathbutdidnotlead toasignificantrescueintheadulteye.However,blockingthelevelsofc-JunNH(2)-terminalkinase(JNK)signalingpathway significantlyrescuedtheneurodegenerationphenotypeofA?42misexpressionbothineyeimaginaldiscaswellastheadult eye.MisexpressionofA?42inducedtranscriptionalupregulationofpuckered(puc),adownstreamtargetandfunctionalread outofJNKsignaling.Moreover,athree-foldincreaseinphospho-Jun(activatedJun)proteinlevelswasseeninA?42retinaas comparedtothewild-typeretina.WhenweblockedbothcaspasesandJNKsignalingsimultaneouslyintheflyretina,the rescueoftheneurodegenerativephenotypeiscomparabletothatcausedbyblockingJNKsignalingpathwayalone. Conclusio