p38γ Mitogen-Activated Protein Kinase Is a Key Regulator in Skeletal Muscle Metabolic Adaptation in Mice 英文参考文献.docVIP

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p38γ Mitogen-Activated Protein Kinase Is a Key Regulator in Skeletal Muscle Metabolic Adaptation in Mice 英文参考文献.doc

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p38γ Mitogen-Activated Protein Kinase Is a Key Regulator in Skeletal Muscle Metabolic Adaptation in Mice 英文参考文献

p38cMitogen-ActivatedProteinKinaseIsaKey RegulatorinSkeletalMuscleMetabolicAdaptationin Mice AndrewR.Pogozelski1,TuoyuGeng1,PingLi1,XinheYin1,VitorA.Lira4,5,MeiZhang1,Jen-TsanChi2,3, ZhenYan1,4,5 * 1DepartmentofMedicine,DukeUniversityMedicalCenter,Durham,NorthCarolina,UnitedStatesofAmerica,2InstituteforGenomeSciencesandPolicy,DukeUniversity MedicalCenter,Durham,NorthCarolina,UnitedStatesofAmerica,3DepartmentofMolecularGeneticsandMicrobiology,DukeUniversityMedicalCenter,Durham,North Carolina,UnitedStatesofAmerica,4DepartmentofMedicine-CardiovascularMedicine,UniversityofVirginia,Charlottesville,Virginia,UnitedStatesofAmerica,5Center forSkeletalMuscleResearchatRobertM.BerneCardiovascularResearchCenter,UniversityofVirginia,Charlottesville,Virginia,UnitedStatesofAmerica Abstract Regularenduranceexerciseinducesskeletalmusclecontractileandmetabolicadaptations,conferringsalutaryhealthbenefits, suchasprotectionagainstthemetabolicsyndrome.Theplasticityofskeletalmusclehasbeenextensivelyinvestigated,but howtheadaptiveprocessesarepreciselycontrolledislargelyunknown.Usingmuscle-specificgenedeletioninmice,wenow showthatp38cmitogen-activatedproteinkinase(MAPK),butnotp38aandp38b,isrequiredforenduranceexercise-induced mitochondrial biogenesis and angiogenesis, whereas none of the p38 isoforms are required for IIb-to-IIa fiber-type transformation. These phenotypic findings were further supported by microarray and real-time PCR analyses revealing contractileactivity-dependentp38ctargetgenes,includingperoxisomeproliferator-activatedreceptorcco-activator-1a(Pgc- 1a) and vascular endothelial growth factor (Vegf), in skeletal muscle following motor nerve stimulation. Gene transfer- mediated overexpression of a dominant negative form of p38c, but not that of p38a or p38b, blocked motor nerve stimulation-inducedPgc-1atranscription.Thesefindingsprovidedirectevidenceforanobligatedroleofp38cMAPK-PGC-1a regulatoryaxisinenduranceexercise-inducedmetabolicadaptation,butnotcontractileadaptation,in