The role of MAP Kinase in adipogenesis from human bone marrow-derived stromal cells

Adipogenesis is a complex process that includes the proliferation of precursor cells, their commitment to the adipogenic lineage and terminal differentiation. This study examined whether or not the ERK signaling pathway regulates the expression or activity of the adipogenic transcription factors during human adipogenesis. The bone marrow-derived stromal cells (BMSCs) were differentiated into adipocytes with the 25 μM troglitazone for 14 days, and aP2 and LPL mRNA were detected. In order to determine the role of the activated ERK during adipogenesis, the BMSCs were exposed to troglitazone and U0126. After inducing differentiation, ERK activity was transiently decreased from 30 min to 6 h in the adipogenic medium and the adipogenic medium plus troglitazone. Those with U0126 markedly inhibited ERK activation. In the presence of troglitazone, the expression of the marker genes increased in a time-dependent manner, and the expression of aP2, LPL and PPARγ genes decreased in the adipogenic BMSCs treated with U0126 in RNA level. The treatment of the adipogenic BMSCs with troglitazone activated C/EBPα and PPARγ, and the U0126 treatment did not affect C/EBPα expression but inhibited PPARγ expression in protein level. In addition, U0126 blocked the change in the adipocyte phenotype. These results suggest that ERK activation is related to PPAR expression but not C/EBPα, and C/EBPα might mediate another pathway in the adipogenesis of BMSCs.