Rosiglitazone-induced adipogenesis in a bone marrow mesenchymal stem cell line

In vitro modeling of adipose tissue is essential for the study of adipogenesis and related diseases as well as for the development of surgical reconstruction procedures and tissue-engineering applications. Peroxisome proliferator activated receptor γ (PPARγ) has been shown to play an integral role in stimulating adipogenesis. There are several established ligands for PPARγ, including rosiglitazone. D1 cells, a multipotential cell line derived from mouse bone marrow, were treated with increasing (0.1, 1, 10, and 30 μM) concentrations of rosiglitazone in DMEM for 48 hours followed by treatment by DMEM alone for up to 15 days. All doses of rosiglitazone stimulated the accumulation of lipids, which was notable by day 6. The adipogenic effect of rosiglitazone was maximized at doses of 10 and 30 μM. Adipogenesis for rosiglitazone-treated cells was greater than that for cells treated with dexamethasone, a conventional method used to stimulate adipogenesis. Significantly higher levels of triglyceride-G (TG) and mature adipocyte markers (PPAR-γ, adipocyte fatty acid-binding protein) were observed with rosiglitazone treatment after 6 days. Cytokines in the supernatants were analyzed by multiplex-based ELISA assays at day 6 after treatment; these cells release adiponectin, resistin, PAI-1, MCP-1, and VEGF with either rosiglitazone or dexamethasone treatment. However, rosiglitazone treatment had lower osteocalcin release than did the control. This study provides evidence that rosiglitazone treatment is a reliable method that can be used to induce adipogenesis of D1 cells, a pluripotential cell line from mouse bone marrow.