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. 2021 Feb 24;12(2):208. doi: 10.1038/s41419-021-03499-w

Fig. 6. MSCs and El-activated CML cell differentiation through JAK2/STAT3 and p38 MAPK pathways.

Fig. 6

A The protein levels of correlated signaling pathways and phosphorylation status were measured by western blotting after treatment with either MSCs or El alone or the combination for 48 h. GAPDH or β-Actin was used as a control. B K562 cells were transfected with siRNA negative control (K562 si-NC) or MPL-siRNA (K562 si-MPL). The K562 si-NC or K562 si-MPL cells were cultured alone or co-cultured with MSCs and El. After 2 days, protein levels of correlated signaling pathways and phosphorylation status were measured by Western blotting. GAPDH was used as a control. C K562 cells were treated with the JAK2 inhibitor TG101209 (TG) (1 μM) followed by co-culturing with MSCs for 48 h. The mRNA expression of differentiation markers was determined by RT-PCR (n = 3). D K562 cells were treated with the STAT3 inhibitor Stattic (5 μM) followed by co-culturing with MSCs for 48 h. The mRNA expression of differentiation markers was determined by RT-PCR (n = 3). E K562 cells were treated with the p38 MAPK inhibitor SB239063 (SB) (10 μM) followed by co-culturing with MSCs for 48 h. The mRNA expression of differentiation markers was determined by RT-PCR (n = 3). All statistical data in this figure represented the mean ± SEM (*P <0.05, **P <0.01, ***P <0.001, ns, not significant, by one-way ANOVA in A and by Student’s t test in B–E). El: eltrombopag, TG: TG101209, SB: SB239063.