ER Stress Induces Anabolic Resistance in Muscle Cells through PKB-Induced Blockade of mTORC1 英文参考文献.docVIP

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ER Stress Induces Anabolic Resistance in Muscle Cells through PKB-Induced Blockade of mTORC1 英文参考文献.doc

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ER Stress Induces Anabolic Resistance in Muscle Cells through PKB-Induced Blockade of mTORC1 英文参考文献

ERStressInducesAnabolicResistanceinMuscleCells throughPKB-InducedBlockadeofmTORC1 LouiseDeldicque1,2,LucBertrand3,AmyPatton4,MarcFrancaux1,KeithBaar4* 1Universite′ catholique de Louvain, Institute of Neuroscience, Research Group in Muscle and Exercise Physiology, Louvain-la-Neuve, Belgium, 2Research Centre for ExerciseandHealth,DepartmentofBiomedicalKinesiology,K.U.Leuven,Leuven,Belgium, 3Universite′ catholiquedeLouvain,InstitutdeRechercheExpe′rimentaleet Clinique,PoleofCardiovascularResearch,Woluwe-Saint-Lambert,Belgium,4DepartmentofNeurobiology,PhysiologyandBehaviour,UniversityofCaliforniaDavis,Davis, California,UnitedStatesofAmerica Abstract Background: Anabolic resistance is the inability to increase protein synthesis in response to an increase in amino acids followingameal.Onepotentialmediatorofanabolicresistanceisendoplasmicreticulum(ER)stress.Thepurposeofthe presentstudywastotestwhetherERstressimpairstheresponsetogrowthfactorsandleucineinmusclecells. Methods:MusclecellswereincubatedovernightwithtunicamycinorthapsigargintoinduceERstressandtheactivationof theunfoldedproteinresponse,mTORC1activityatbaselineandfollowinginsulinandaminoacids,aswellasaminoacid transportweredetermined. Results:ERstressdecreasedbasalphosphorylationofPKBandS6K1inadose-dependentmanner.Inspiteofthedecreasein basal PKB phosphorylation, insulin (10–50nM) could still activate both PKB and S6K1. The leucine (2.5–5mM)-induced phosphorylationofS6K1ontheotherhandwasrepressedbylowconcentrationsofbothtunicamycinandthapsigargin.To determine the mechanism underlying this anabolic resistance, several inhibitors of mTORC1 activation were measured. TunicamycinandthapsigargindidnotchangethephosphorylationorcontentofeitherAMPKorJNK,bothincreasedTRB3 mRNA expression and thapsigargin increased REDD1 mRNA. Tunicamycin and thapsigargin both decreased the basal phosphorylationstateofPRAS40.NeithertunicamycinnorthapsigarginpreventedphosphorylationofPRAS40byinsulin. However, since PKB is not activated b