2011
Recent progress in understanding molecular mechanisms of cartilage degeneration during osteoarthritis
Wang M, Shen J, Jin H, Im H, Sandy J, Chen D. Recent progress in understanding molecular mechanisms of cartilage degeneration during osteoarthritis. Annals Of The New York Academy Of Sciences 2011, 1240: 61-69. PMID: 22172041, PMCID: PMC3671949, DOI: 10.1111/j.1749-6632.2011.06258.x.Peer-Reviewed Original ResearchConceptsMolecular mechanismsEffective disease-modifying treatmentDisease-modifying treatmentsIndian hedgehogCell typesMolecular levelExtracellular matrixΒ-cateninMutant miceOA patientsJoint injuryRecent findingsOA developmentHIF-2aTGF-β1Biomechanical alterationsOA subtypesCartilage degenerationPrevalent diseaseOsteoarthritisPathwayVivo studiesReceptor ligandsAmerican adultsADAMTS4/5BMP2, but not BMP4, is crucial for chondrocyte proliferation and maturation during endochondral bone development
Shu B, Zhang M, Xie R, Wang M, Jin H, Hou W, Tang D, Harris SE, Mishina Y, O'Keefe RJ, Hilton MJ, Wang Y, Chen D. BMP2, but not BMP4, is crucial for chondrocyte proliferation and maturation during endochondral bone development. Journal Of Cell Science 2011, 124: 3428-3440. PMID: 21984813, PMCID: PMC3196857, DOI: 10.1242/jcs.083659.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBone DevelopmentBone Morphogenetic Protein 2Bone Morphogenetic Protein 4Cell DifferentiationCell Growth ProcessesCells, CulturedChondrocytesCore Binding Factor Alpha 1 SubunitCyclin-Dependent Kinase 4Gene Expression RegulationGrowth PlateMiceMice, KnockoutOsteochondrodysplasiasProtein Processing, Post-TranslationalSignal TransductionConceptsEndochondral bone developmentBMP4 geneCartilage developmentDeletion of Bmp2Post-transcriptional levelRunx2 protein levelsBone developmentChondrocyte proliferationChondrodysplasia phenotypeProteasomal degradationBMP2 geneGenetic controlKey regulatorConditional knockout miceMolecular mechanismsKnockout miceBMP2Chondrocyte differentiationGenesGrowth plate chondrocytesRunx2 expressionCartilage phenotypeSpecific functionsProfound defectsNovel insights
2010
Smad3 Prevents β-Catenin Degradation and Facilitates β-Catenin Nuclear Translocation in Chondrocytes*
Zhang M, Wang M, Tan X, Li TF, Zhang YE, Chen D. Smad3 Prevents β-Catenin Degradation and Facilitates β-Catenin Nuclear Translocation in Chondrocytes*. Journal Of Biological Chemistry 2010, 285: 8703-8710. PMID: 20097766, PMCID: PMC2838293, DOI: 10.1074/jbc.m109.093526.Peer-Reviewed Original ResearchConceptsBeta-catenin protein stabilityBeta-catenin nuclear translocationNuclear translocationDownstream target genesBeta-catenin proteinN-terminal regionDetailed molecular mechanismsΒ-catenin degradationTGF-beta/Smad3Β-catenin nuclear translocationProtein complexesProtein stabilityTarget genesRegulatory mechanismsSmad3 interactionMolecular mechanismsChondrocyte developmentDependent degradationNovel mechanismDependent mannerWntSmad3Growth factorTranslocationPathway