Dissociation of Progressive Dopaminergic Neuronal Death and Behavioral Impairments by Bax Deletion in a Mouse Model of Parkinsons Diseases 英文参考文献.docVIP

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Dissociation of Progressive Dopaminergic Neuronal Death and Behavioral Impairments by Bax Deletion in a Mouse Model of Parkinsons Diseases 英文参考文献.doc

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Dissociation of Progressive Dopaminergic Neuronal Death and Behavioral Impairments by Bax Deletion in a Mouse Model of Parkinsons Diseases 英文参考文献

DissociationofProgressiveDopaminergicNeuronal DeathandBehavioralImpairmentsbyBaxDeletionina MouseModelofParkinson’sDiseases TaeWooKim1,YounghyeMoon1,2,KyungjinKim2,JeongEunLee3,HyunChulKoh3,ImJooRhyu1 ,Hyun Kim1,WoongSun1* 1BK21Program,DepartmentofAnatomy,KoreaUniversityCollegeofMedicine,Sungbuk-Gu,Seoul,Korea,2DepartmentofBiologicalSciences,SeoulNationalUniversity, Seoul,Korea,3DepartmentofPharmacology,CollegeofMedicine,HanyangUniversity,Seoul,Korea Abstract Parkinson’s disease (PD) is a common, late-onset movement disorder with selective degeneration of dopaminergic (DA) neurons in the substantia nigra (SN). Although the neurotoxin 6-hydroxydopamine (6-OHDA) has been used to induce progressivedegenerationofDAneuronsinvariousanimalmodelsofPD,theprecisemolecularpathwayandtheimpactof anti-apoptotic treatment on this neurodegeneration are less understood. Following a striatal injection of 6-OHDA, we observedatrophyandprogressivedeathofDAneuronsinwild-typemice.ThesedegeneratingDAneuronsneverexhibited signsofapoptosis(i.e.,caspase-3activationandcytoplasmicreleaseofcytochromeC),butrathershownucleartranslocation of apoptosis-inducing factor (AIF), a hallmark of regulated necrosis. However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocationofAIF,indicatingthat6-OHDA-inducedDAneuronaldeathismediatedbyBax-dependentAIFactivation.On the other hand, DA neurons that survived in Bax-KO mice exhibited marked neuronal atrophy, without significant improvementofPD-relatedbehavioraldeficits.Thesefindingssuggestthatanti-apoptotictherapymaynotbesufficientfor PDtreatment,andthepreventionofBax-independentneuronalatrophymaybeanimportanttherapeutictarget. Citation:KimTW,MoonY,KimK,LeeJE,KohHC,etal.(2011)DissociationofProgressiveDopaminergicNeuronalDeathandBehavioralImpairmentsbyBax DeletioninaMouseModelofParkinson’sDiseases.PLoSONE6(10):e25346.doi:10.1371/journal.pone.0025346 Editor:Koic