C-Jun N-Terminal Kinase 2 Promotes Liver Injury via the Mitochondrial Permeability Transition after Hemorrhage and Resuscitation英文文献资料.docVIP

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C-Jun N-Terminal Kinase 2 Promotes Liver Injury via the Mitochondrial Permeability Transition after Hemorrhage and Resuscitation英文文献资料.doc

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C-Jun N-Terminal Kinase 2 Promotes Liver Injury via the Mitochondrial Permeability Transition after Hemorrhage and Resuscitation英文文献资料

HindawiPublishingCorporation HPBSurgery Volume2012,ArticleID641982,9pages doi:10.1155/2012/641982 ResearchArticle C-JunN-TerminalKinase2PromotesLiverInjury viatheMitochondrialPermeabilityTransitionafter HemorrhageandResuscitation EduardoN.Maldonado, MarkLehnert, ChristophCzerny,1,2TomP.Theruvath,1 1 2 IngoMarzi, ZhiZhong, 2 1andJohnJ.Lemasters 1,3 1 CenterforCellDeath,InjuryRegeneration,DepartmentsofPharmaceuticalBiomedicalSciences, MedicalUniversityofSouthCarolina,Charleston,SC29425,USA 2 3 DepartementofTraumaSurgery,J.W.GoetheUniversityFrankfurtamMain,60590FrankfurtamMain,Germany BiochemistryMolecularBiology,MedicalUniversityofSouthCarolina,MSC140,Charleston,SC29425,USA CorrespondenceshouldbeaddressedtoJohnJ.Lemasters,jjlemasters@ Received16February2012;Accepted24March2012 AcademicEditor:PeterSchemmer Copyright?2012ChristophCzernyetal. This is an open access article distributed under the Creative Commons Attribution License,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperly cited. Hemorrhagic shock leads to hepatic hypoperfusion and activation of mitogen-activated stress kinases (MAPK) like c-Jun N- terminalkinase(JNK)1and2.Ouraimwastodeterminewhethermitochondrialdysfunctionleadingtohepaticnecrosisand apoptosisafterhemorrhage/resuscitation(H/R)wasdependentonJNK2.Underpentobarbitalanesthesia,wildtype (WT)and JNK2de?cient(KO)micewerehemorrhagedto30mmHgfor3handthenresuscitatedwithshedbloodplushalfthevolume oflactatedRinger’ssolution.Serumalanineaminotransferase(ALT),necrosis,apoptosisandoxidativestresswereassessed6h afterresuscitation.Mitochondrialpolarizationwasassessedbyintravitalmicroscopy.AfterH/R,ALTinWT-miceincreasedfrom 130U/Lto4800U/L.InKO-mice,ALTafterH/Rwasbluntedto1800U/l(P 0.05).Necrosis,caspase-3activityandROSwere allsubstantiallydecreasedinKOcomparedtoWTmiceafterH/R.Aftershamoperation,intravitalmicroscopyrevealedpunctate mitochondrial