Fig. 7

Graphical summary of the investigated signaling pathways during osteogenic differentiation of DFCs. The osteogenic differentiation in DFCs can be induced by dexamethasone or BMP2. Induction by dexamethasone leads to downregulation of classical PKCs, while induction by BMP2 inhibits both classical PKCs and Akt. Activity of classical PKCs is sustained by PTHrP and can be inhibited by Wnt5a. In osteogenic differentiating cells, classical PKCs inhibit the activity of Akt, while Akt was shown to inhibit the NF-κB pathway and sustain the activity of β-catenin by phosphorylation and thereby inhibition of GSK3β. Classical PKCs stimulate the NF-κB pathway. Eventually, the transcription factors NF-κB and β-catenin modulate the osteogenic differentiation of DFCs. Furthermore, the BMP2/Smad signaling pathway, which is pivotal for BMP2-induced osteogenic induction, is disturbed by Akt