Involvement of PPAR γ in senescence-induced osteoporosis

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Senescence-induced osteoporosis is thought to be a low turnover type and to be due to the shift from osteoblastogenesis to adipogenesis. In this study, we investigated the effects of some drugs affected bone metabolism on adipose differentiation and the effects of adipogenesis on osteoclastogenesis and osteoblastogenesis. We used mouse preosteoblast cell lines established in our laboratory and human mesenchymal stem cells isolated from bone marrow. The PPARγ ligands such as 15-deoxy.-Δ 12,14-PGJ2 and trogritazone stimulated adipogenesis, but IL-11 and vitaminK2 suppressed the adipogenesis. The adipocyte differentiation caused to decrease the osteoclast formation-supporting activity, but did not affect osteoblastogenesis. The similar results were obtained from in vivo study. When human mesenchymal cells with BMP-2 and vitamin K2 inoculated to Matrigel and transplanted subcutaneously to nude mice, the cells was differentiated to osteoblasts and adipocytes by BMP-2. The effect of vitamin K2 on osteoblastogenesis failed to be observed in spite of the suppression of adipogenesis.These data indicate that the suppression of adipogenesis is not benefit for the protect of senescence-induced osteoporosis.