AKT Signaling Mediates IGF-I Survival Actions on Otic Neural Progenitors 英文参考文献.docVIP

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AKT Signaling Mediates IGF-I Survival Actions on Otic Neural Progenitors 英文参考文献.doc

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AKT Signaling Mediates IGF-I Survival Actions on Otic Neural Progenitors 英文参考文献

AKTSignalingMediatesIGF-ISurvivalActionsonOtic NeuralProgenitors MariaR.Aburto1,2,MartaMagarin?os1,2,3,YolandaLeon1,3,IsabelVarela-Nieto1,2*.,HortensiaSanchez- Calderon1,2. 1InstitutodeInvestigacionesBiomedicas‘‘AlbertoSols’’,CSIC-UAM,Madrid,Spain,2CIBERER,Unit761,ISCIII,Madrid,Spain,3DepartamentodeBiologia,Universidad AutonomadeMadrid,Madrid,Spain Abstract Background:Oticneuronsandsensorycellsderivefromcommonprogenitorswhosetransitionintomaturecellsrequires thecoordinationofcellsurvival,proliferationanddifferentiationprogrammes.Neurotrophicsupportandsurvivalofpost- mitoticoticneuronshavebeenintensivelystudied,butthebasesunderlyingtheregulationofprogrammedcelldeathin immatureproliferativeoticneuroblastsremainspoorlyunderstood.TheproteinkinaseAKTactsasanode,playingacritical roleincontrollingcellsurvivalandcellcycleprogression.AKTisactivatedbytrophicfactors,includinginsulin-likegrowth factor I (IGF-I), through the generation of the lipidic second messenger phosphatidylinositol 3-phosphate by phosphatidylinositol 3-kinase (PI3K). Here we have investigated the role of IGF-dependent activation of the PI3K-AKT pathwayinmaintenanceofoticneuroblasts. Methodology/PrincipalFindings:Byusingacombinationoforganotypicculturesofchicken(Gallusgallus)oticvesiclesand acoustic-vestibularganglia,Westernblotting,immunohistochemistryandinsituhybridization,weshowthatIGF-I-activation ofAKTprotectsneuralprogenitorsfromprogrammedcelldeath.IGF-Imaintainsoticneuroblastsinanundifferentiatedand proliferative state, which is characterised by the upregulation of the forkhead box M1 (FoxM1) transcription factor. By contrast, our results indicate that post-mitotic p27Kip-positive neurons become IGF-I independent as they extend their neuronalprocesses. Neuronsgraduallyreducetheirexpressionof theIgf1r,whiletheyincrease thatof theneurotrophin receptor,TrkC. Conclusions/Significance:ProliferativeoticneuroblastsaredependentontheactivationofthePI3K-AKTpathwaybyIGF-I forsurvivalduringtheoticneuro