Figure 1

Dexamethasone (Dex) induces the osteogenic differentiation of stem cells by increasing the transcription of FHL-2. Binding of FHL-2 to β-catenin potentiates the transport of β-catenin to the nucleus, where it binds TCF/LEF-1 (T-cell factor/lymphoid enhancer factor) and leads to the transcription of Runx2. Dex also contributes to osteogenic differentiation by increasing the expression of the Runx2 co-activator TAZ. Additionally, Dex treatment induces the expression of the gene encoding MKP-1 (a component of the mitogen-activated protein kinase (MAPK) signaling pathway), which dephosphorylates and thereby activates the key transcription factor Runx2 via extracellular related kinase (ERK) signaling. The addition of ascorbic acid (Asc) facilitates osteogenic differentiation by increasing secretion of collagen type I (Col1), resulting in increased binding of α2β1 integrins to Col1. This leads to the phosphorylation of ERK1/2 in the MAPK signaling pathway, and a subsequent translocation of P-ERK1/2 to the nucleus where it activates Runx2 by phosphorylation. Abbreviations: ECM, extracellular matrix; +OH, hydroxylation; MEK, MAPK/ERK Kinase; FAK, Focal Adhesion Kinase; P, phosphate.