拉力軟骨細(xì)胞

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1、In?amm.Res.(2015)64:243–252DOI10.1007/s00011-015-0804-2In?ammationResearchORIGINALRESEARCHPAPERHyaluronansuppressesmechanicalstress-inducedexpression ofcatabolicenzymesbyhumanchondrocytesviainhibition ofIL-1bproductionandsubsequentNF-jBactivationMasatsuguOzawa?KeiichiroNishida

2、?AkiYoshida?TaichiSaito? RyozoHarada?TakahiroMachida?ToshifumiOzakiReceived:23August2014/Revised:25January2015/Accepted:10February2015/Publishedonline:19February2015óSpringerBasel2015AbstractResultsHAinhibitedmRNAexpressionofADAMTS-4,ObjectiveToinvestigatetheinhibitoryeffectof

3、hyalur-onan(HA)onmechanicalstress-inducedexpressionofa-5,andMMP13viainhibitionofIL-1bsecretionandNF-jBactivation.However,HAfailedtodisintegrinandmetalloproteinasewiththrombospondininhibitCTS-inducedRUNX-2expressionandsubsequenttype1motifs(ADAMTS)-4,-5andmatrixmetalloprotei-exp

4、ressionofADAMTS-5andMMP-13afterCTS.nase(MMP)-13byhumanchondrocytes.ConclusionsOurresultsdemonstratedthatHAsig-MaterialsandmethodsNormalhumanarticularchon-ni?cantlysuppressedmechanicalstress-inducedexpressiondrocyteswerepre-incubatedwithorwithout1.0mg/mLHA(2700kDa)for12hat37°Ci

5、nstretchchambers,thenofcatabolicproteasesbyinhibitionoftheNF-jB–IL-1bpathway,butdidnotsuppressmechanicalstress-inducedtheywereexposedtouni-axialcyclictensilestrain(CTS,RUNX-2signaling.)..Theconcentra-tionofIL-1binthesupernatantwasmeasuredusingenzyme-linkedimmunosorbentassay(EL

6、ISA).KeywordsChondrocyteáHyaluronanáMechanicalstressáAggrecanaseáNF-jBáRUNX-2Introduction,andOsteoarthritis(OA)isoneofthemostcommonjointdis-eases,andthenumberofpatientswithOAiscontinuouslyincreasing[1].Hyaluronan(HA),apolysaccharidecon-ResponsibleEditor:YoshiyaTanaka.sistingof

7、alongchainofdisaccharides,isanaturalcomponentofcartilageandsynovial?uid,andisknowntoM.OzawaáA.YoshidaáR.HaradaáT.MachidaáT.OzakiDepartmentofOrthopaedicSurgery,OkayamaUniversityGraduateSchoolofMedicine,DentistryandPharmaceuticalSciences,2-5-1Shikata-cho,OkayamaCity,Okayama700-8

8、558,Japanactasashockabsorberinthearticularenvironment[2,3].HA