cyclin-d1 and 2-(4-morpholinoanilino)-6-cyclohexylaminopurine

Articular chondrocytes derived from osteoarthritic tissues (OA HAC) show a severely reduced chondrogenic commitment. This impairment undermines their use for tissue-engineered cartilage repair, which relies on cell proliferation and growth to meet therapeutic needs, but also on efficient cell plasticity to recover the chondrogenic phenotype. Reversine (Rev), a 2,6-disubstituted purine inhibitor of spindle-assembly checkpoints, was described to convert differentiated mesenchymal cells to their undifferentiated precursors. We hypothesized that Rev exposure could divert OA HAC to more plastic cells, re-boosting their subsequent commitment. HAC were enzymatically released from OA cartilage specimens, expanded for 2 weeks and treated with 5 μm Rev in dimethylsulphoxide (DMSO) or with DMSO alone for 6 days. Cell growth was assessed using the AlamarBlue

Topics: Aged; Aged, 80 and over; Cartilage, Articular; Cell Cycle Checkpoints; Cell Proliferation; Cell Shape; Cells, Cultured; Chondrocytes; Cyclin D1; Dimethyl Sulfoxide; Female; Gene Expression Regulation; Humans; Ki-67 Antigen; Male; Morpholines; Osteoarthritis; Phenotype; Purines; RNA, Messenger; Smad3 Protein; SOX9 Transcription Factor