2012
Lead induces an osteoarthritis‐like phenotype in articular chondrocytes through disruption of TGF‐β signaling
Holz JD, Beier E, Sheu T, Ubayawardena R, Wang M, Sampson ER, Rosier RN, Zuscik M, Puzas JE. Lead induces an osteoarthritis‐like phenotype in articular chondrocytes through disruption of TGF‐β signaling. Journal Of Orthopaedic Research® 2012, 30: 1760-1766. PMID: 22517267, PMCID: PMC3839422, DOI: 10.1002/jor.22117.Peer-Reviewed Original ResearchConceptsLead treatmentOsteoarthritis-like phenotypeNormal chondrocyte phenotypeDose-dependent mannerArticular chondrocytesTGF-β signalingActive caspase-3MMP13 activityLead exposureHigher level leadType II collagenVivo exposureCollagen levelsNovel targetType X collagenCaspase-3Articular surfaceEnvironmental toxinsLead toxicityII collagenReporter activityTreatmentArticular cartilageDosePhenotypic shift
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