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We recently reported that cilostazol protects chondrocytes against stress-inducedapoptosis and prevents cartilage destruction in an osteoarthritis (OA) model.In the present study, we elucidate the mechanism underlying the protective effectinduced by cilostazol against stress-induced apoptosis in chondrocytes. Cilostazolsignificantly reduced the expression of type II collagen and stimulated the accumulationof β-catenin in primary rat articular chondrocytes. Moreover, cilostazol-inducedchondrocytes showed induction of senescent phenotypes, such as changes in cellmorphology, decrease in cell proliferation and increase in specific senescence-associatedβ-galactosidase (SA-β-gal) staining. Moreover, dedifferentiated chondrocytes obtainedby serial subculture showed cellular senescence that increased with passage number.In addition, the percentage of terminal dUTP nick end-labeling (TUNEL)-positivecells was higher when chondrocytes were treated with cilostazol and the apoptosisinducer etoposide than when the cells were treated with etoposide alone. Our findingssuggest that cilostazol induces dedifferentiation and senescence in rat articularchondrocytes and renders them resistant to etoposide-induced apoptosis.

Cilostazol induces cellular senescence and confers resistance to etoposide-induced apoptosis in articular chondrocytes