Disruption of Astrocyte STAT3 Signaling Decreases Mitochondrial Function and Increases Oxidative Stress In Vitro 英文参考文献.docVIP

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Disruption of Astrocyte STAT3 Signaling Decreases Mitochondrial Function and Increases Oxidative Stress In Vitro 英文参考文献.doc

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Disruption of Astrocyte STAT3 Signaling Decreases Mitochondrial Function and Increases Oxidative Stress In Vitro 英文参考文献

DisruptionofAstrocyteSTAT3SignalingDecreases MitochondrialFunctionandIncreasesOxidativeStressIn Vitro TheodoreA.Sarafian1*,CindyMontes1,TetsuyaImura1,JingweiQi1,GiovanniCoppola2,DanielH. Geschwind2,MichaelV.Sofroniew1 1DepartmentofNeurobiology,DavidGeffenSchoolofMedicine,UniversityofCaliforniaLosAngeles,LosAngeles,California,UnitedStatesofAmerica,2Departmentof Neurology,TheSemelInstituteforNeuroscienceandHumanBehavior,DavidGeffenSchoolofMedicine,UniversityofCaliforniaLosAngeles,California,UnitedStatesof America Abstract Background:Astrocytesexertawidevarietyoffunctionsinhealthanddiseaseandrespondtoawiderangeofsignaling pathways,includingmembersoftheJanus-kinasesignaltransducersandactivatorsoftranscription(Jak-STAT)family.We haverecentlyshownthatSTAT3isanimportantregulatorofastrocytereactivityafterspinalcordinjuryinvivo[1]. Methodology/Principal Findings: Here, we used both a conditional gene deletion strategy that targets the deletion of STAT3selectivelytoastrocytes(STAT3-CKO),andapharmacologicalinhibitorofJAK-2,AG490,inculturedastrocytesinvitro, toinvestigatepotentialfunctionsandmoleculesinfluencedbySTAT3signalinginrelationtomitochondrialfunctionand oxidativestress.OurfindingsshowthattheabsenceofSTAT3signalinginastrocytesleadsto(i)increasedproductionof superoxide anion and other reactive oxygen species and decreased level of glutathione, (ii) decreased mitochondrial membranepotentialanddecreasedATPproduction,and(iii)decreasedrateofcellproliferation.Manyofthedifferences observedinSTAT3-CKOastrocytesweredistinctlyalteredbyexposuretorotenone,suggestingaroleforcomplexIofthe mitochondrial electron transport chain. Gene expression microarray studies identified numerous changes in STAT3-CKO cellsthatmayhavecontributedtotheidentifieddeficitsincellfunction. Conclusions/Significance: Takentogether,theseSTAT3-dependentalterationsincellfunctionandgeneexpressionhave relevancetobothreactivegliosisandtothesupportandprotectionofsurroundingcellsinneuraltissue. Citation:SarafianTA