Fig. 3

Stimulation of signal transduction in FGF-2-treated hASCs through multi-signaling pathways. After incubation in serum-free DMEM for 18 h, cells were treated with inhibitors at the designated concentrations [Erk1/2 inhibitor (PD98059, 5 μM), JNK inhibitor (SP600125, 10 μM), p38 MAPK inhibitor (SB203580, 20 μM), or PI3K/Akt inhibitor (LY294002, 10 μM)]. Cell proliferation was assessed with a Cell Counting Kit-8 after culturing with inhibitors for 48 h, and cellular proteins were extracted after cells were treated with FGF-2 with/without FGFR inhibitor NVP-BGJ398 (0.1 μM) for 5 min. Inhibitors were added 1 h prior to stimulation with FGF-2 (5 ng/ml). a Pharmacological inhibition of FGF-2-mediated proliferation through Erk1/2, JNK, p38 MAPK, and Akt pathways (n = 5). *p < 0.01 compared with no inhibitor. b Immunoblots of p-Akt, p-Erk1/2, p-p38 MAPK, and p-JNK in cells treated with FGF-2 with/without NVP-BGJ398