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Fig. 6. Involvement of NFATc1 in the reversion of differentiation by JNK inhibition. (A) RAW264.7 cells were transfected with NFAT-reporter luciferase plasmid and stimulated with RANKL for 24 hours in the presence or absence of SP600125 (SP, 10 µM). Luciferase activity was assessed with cell lysates. (B,C) BMM-derived pOCs were treated with or without SP600125 (10 µM) for 24 hours. The mRNA (B) and protein (C) levels of NFATc1 were determined by reverse transcriptase (RT)-PCR and western blotting analyses, respectively. (D-F) pOCs were infected with NFATc1 siRNA or control siRNA (Luc) retroviruses. (D) The reduced level of NFATc1 was determined by western blotting. (E) Infected cells were cultured with RANKL (100 ng/ml) and M-CSF (30 ng/ml) for 24 hours before TRAP-staining. (F) The percentage of TRAP+ cells was assessed. (G,H) pOCs were infected with active NFATc1 or control retroviruses and incubated with or without SP600125 (10 µM) in the presence of RANKL and M-CSF for 24 hours. The percentage of TRAP+ cells was determined. (A,F,H) Data are mean ± s.d. of triplicate samples. All results are representative of three independent experiments.
