Transglutaminase 2 cross-linking activity is linked to invadopodia formation and cartilage breakdown in arthritis 英文参考文献.docVIP

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Transglutaminase 2 cross-linking activity is linked to invadopodia formation and cartilage breakdown in arthritis 英文参考文献.doc

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Transglutaminase 2 cross-linking activity is linked to invadopodia formation and cartilage breakdown in arthritis 英文参考文献

Lauzieretal.ArthritisResearchTherapy2012,14:R159 /content/14/4/R159 RESEARCH ARTICLE OpenAccess Transglutaminase2cross-linkingactivityislinked toinvadopodiaformationandcartilage breakdowninarthritis AnnieLauzier,MartineCharbonneau,MarilènePaquette,KellyHarperandClaireMDubois* Abstract Introduction:Themicroenvironmentsurroundinginflamedsynoviumleadstotheactivationoffibroblast-like synoviocytes(FLSs),whichareimportantcontributorstocartilagedestructioninrheumatoidarthritic(RA)joints. Transglutaminase2(TG2),anenzymeinvolvedinextracellularmatrix(ECM)cross-linkingandremodeling,is activatedbyinflammatorysignals.ThisstudywasundertakentoassessthepotentialcontributionofTG2toFLS- inducedcartilagedegradation. Methods:Transglutaminase(TGase)activityandcollagendegradationwereassessedwiththe immunohistochemistryofcontrol,collagen-inducedarthritic(CIA)orTG2knockdown(shRNA)-treatedjointtissues. TGaseactivityincontrol(C-FLS)andarthritic(A-FLS)ratFLSswasmeasuredbyinsitu5-(biotinamido)-pentylamine incorporation.InvadopodiaformationandfunctionsweremeasuredinratFLSsandcellsfromnormal(control;C- FLS)andRApatients(RA-FLS)byinsituECMdegradation.Immunoblotting,enzyme-linkedimmunosorbentassay (ELISA),andp3TP-Luxreporterassayswereusedtoassesstransforminggrowthfactor-b(TGF-b)productionand activation. Results:TG2andTGaseactivitywereassociatedwithcartilagedegradationinCIAjoints.Incontrast,TGaseactivity andcartilagedegradationwerereducedinjointsbyTG2knockdown.A-FLSsdisplayedhigherTGaseactivityand TG2expressioninECMthandidC-FLSs.TG2knockdownorTGaseinhibitionresultedinreducedinvadopodia formationinratandhumanarthriticFLSs.Incontrast,increasedinvadopodiaformationwasnotedinresponseto TGaseactivityinducedbyTGF-b,dithiothreitol(DTT),orTG2overexpression.TG2-inducedincreasesininvadopodia formationwereblockedbyTGF-bneutralizationorinhibitionofTGF-bR1. Conclusions:TG2,throughitsTGaseactivity,isrequiredforECMdegradationinarthriticFLSandCIAjoints.Our findingsprovideapotentialtargettopreventcartilagedegrada