2014
Activation of β-catenin signalling leads to temporomandibular joint defects
Wang M, Li S, Xie W, Shen J, Im H, Holz J, Wang M, Diekwisch T, Chen D. Activation of β-catenin signalling leads to temporomandibular joint defects. ECells & Materials 2014, 28: 223-235. PMID: 25340802, PMCID: PMC4288590, DOI: 10.22203/ecm.v028a15.Peer-Reviewed Original ResearchConceptsDouble mutant miceTMJ disordersΒ-cateninMutant miceADAMTS5-/- miceRole of MMP13OA-like phenotypeTemporomandibular joint disordersMG reporter micePotential therapeutic targetDevelopment of TMJTMJ cartilage degenerationHip osteoarthritisTMJ samplesJoint disordersTherapeutic targetReporter miceTransgenic miceCartilage degenerationMiceTMJ cartilageADAMTS5 geneTMJADAMTS5MMP13
2012
Conditional activation of β‐catenin signaling in mice leads to severe defects in intervertebral disc tissue
Wang M, Tang D, Shu B, Wang B, Jin H, Hao S, Dresser KA, Shen J, Im H, Sampson ER, Rubery PT, Zuscik MJ, Schwarz EM, O'Keefe RJ, Wang Y, Chen D. Conditional activation of β‐catenin signaling in mice leads to severe defects in intervertebral disc tissue. Arthritis & Rheumatism 2012, 64: 2611-2623. PMID: 22422036, PMCID: PMC3632450, DOI: 10.1002/art.34469.Peer-Reviewed Original ResearchConceptsDisc degenerationΒ-cateninDisc tissueExtensive osteophyte formationLow back painDisc tissue samplesIntervertebral disc degenerationPolymerase chain reaction assaysTissue functionBack painReal-time polymerase chain reaction assaysRunt-related transcription factorΒ-catenin protein levelsChain reaction assaysIntervertebral disc tissueOsteophyte formationΒ-catenin levelsImmunohistochemical analysisNormal subjectsMatrix metalloproteinase-13 inhibitorsTransgenic miceHistologic analysisΒ-catenin proteinADAMTS5 expressionGenetic ablation
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 adultsADAMTS4/5
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