Apelin Deficiency Accelerates the Progression of Amyotrophic Lateral Sclerosis 英文参考文献.docVIP

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Apelin Deficiency Accelerates the Progression of Amyotrophic Lateral Sclerosis 英文参考文献.doc

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Apelin Deficiency Accelerates the Progression of Amyotrophic Lateral Sclerosis 英文参考文献

ApelinDeficiencyAcceleratestheProgressionof AmyotrophicLateralSclerosis AtsushiKasai1,3*,ToshihikoKinjo1,RieIshihara1,IkumiSakai1,YukiIshimaru1,YasuhiroYoshioka1, AkikoYamamuro1,KumikoIshige2,YoshihisaIto2,SadaakiMaeda1 1DepartmentofPharmacotherapeutics,FacultyofPharmaceuticalSciences,SetsunanUniversity,Hirakata,Osaka,Japan,2LaboratoryofPharmacology,Departmentof Pharmacy,SchoolofPharmacy,NihonUniversity.Funabashi,Chiba,Japan,3DepartmentofPsychiatry,SemelInstituteforNeuroscienceandHumanBehavior,University ofCaliforniaLosAngeles,LosAngeles,California,UnitedStatesofAmerica Abstract Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the selective loss of motor neurons. Recentstudieshaveimplicatedthatchronichypoxiaandinsufficientvascularendothelialgrowthfactor(VEGF)-dependent neuroprotectionmayleadtothedegenerationofmotorneuronsinALS.Expressionofapelin,anendogenousligandforthe Gprotein-coupledreceptorAPJ,isregulatedbyhypoxia.Inaddition,recentreportssuggestthatapelinprotectsneurons against glutamate-induced excitotoxicity. Here, we examined whether apelin is an endogenous neuroprotective factor usingSOD1G93A mousemodelofALS.InmouseCNStissues,thehighestexpressionsofbothapelinandAPJmRNAswere detectedinspinalcord.APJimmunoreactivitywasobservedinneuronalcellbodieslocatedingraymatterofspinalcord. AlthoughapelinmRNAexpressioninthespinalcordofwild-typemicewasnotchangedfrom4to18weeksage,thatof SOD1G93Amicewasreducedalongwiththeparalyticphenotype.Inaddition,doublemutantapelin-deficientandSOD1G93A displayedthediseasephenotypesearlierthanSOD1G93A littermates.Immunohistochemicalobservationrevealedthatthe number of motor neurons was decreased and microglia were activated in the spinal cord of the double mutant mice, indicating that apelin deficiency pathologically accelerated the progression of ALS. Furthermore, we showed that apelin enhancedtheprotectiveeffectofVEGFon H2O2-inducedneuronaldeathin primaryneurons.Theseresultssuggestthat apelin/A