CEBPβ Promotes Transition from Proliferation to Hypertrophic Differentiation of Chondrocytes through Transactivation of p57Kip2 英文参考文献.docVIP

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CEBPβ Promotes Transition from Proliferation to Hypertrophic Differentiation of Chondrocytes through Transactivation of p57Kip2 英文参考文献.doc

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CEBPβ Promotes Transition from Proliferation to Hypertrophic Differentiation of Chondrocytes through Transactivation of p57Kip2 英文参考文献

C/EBPbPromotesTransitionfromProliferationto HypertrophicDifferentiationofChondrocytesthrough Transactivationofp57Kip2 MakotoHirata1.,FumitakaKugimiya1.,AtsushiFukai1,ShinsukeOhba2,NaohiroKawamura1, ToruOgasawara1,YosukeKawasaki1,TakuSaito1,FumikoYano2,ToshiyukiIkeda1,KozoNakamura1, Ung-ilChung2,HiroshiKawaguchi1* 1DepartmentsofSensory Motor System Medicine, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan, 2Centerfor Disease Biology andIntegrative Medicine,FacultyofMedicine,UniversityofTokyo,Bunkyo-ku,Tokyo,Japan Abstract Background: Although transition from proliferation to hypertrophic differentiation of chondrocytes is a crucial step for endochondral ossification in physiological skeletal growth and pathological disorders like osteoarthritis, the underlying mechanismremainsanenigma.ThisstudyinvestigatedtheroleofthetranscriptionfactorCCAAT/enhancer-bindingprotein b(C/EBPb)inchondrocytesduringendochondralossification. Methodology/PrincipalFindings:MouseembryoswithhomozygousdeficiencyinC/EBPb(C/EBPb2/2)exhibiteddwarfism withelongatedproliferative zoneanddelayedchondrocyte hypertrophy inthegrowthplatecartilage.Inthecultures of primary C/EBPb2/2 chondrocytes, cell proliferation was enhanced while hypertrophic differentiation was suppressed. Contrarily,retroviraloverexpressionofC/EBPbinchondrocytessuppressedtheproliferationandenhancedthehypertrophy, suggesting the cell cycle arrest by C/EBPb. In fact, a DNA cell cycle histogram revealed that the C/EBPb overexpression causedaccumulationofcellsintheG0/G1fraction.Amongcellcyclefactors,microarrayandreal-timeRT-PCRanalyseshave identifiedthecyclin-dependentkinaseinhibitorp57Kip2asthetranscriptionaltargetofC/EBPb.p57Kip2wasco-localizedwith C/EBPbinlateproliferativeandpre-hypertrophicchondrocytesofthemousegrowthplate,whichwasdecreasedbytheC/ EBPbdeficiency.Luciferase-reporterandelectrophoreticmobilityshiftassaysidentifiedthecoreresponsiveelementofC/ EBPbinthep57Kip2 promoterbetween2150and2130bpregio