Inhibiting p38 MAPK-STAT1 significantly rescued Wip1 deficiency-caused accelerated neutrophil development. (A) Sorted WT GMPs were treated with G-CSF in the presence or absence of 10μM anisomycin (activator of p38 and Jnk) and/or 100nM SP600125 (inhibitor of Jnk). The transcriptional factor C/EBPα mRNA expression was detected by real-time PCR. One photographed CFU (B), neutrophil number per CFU (C), number of CFUs (D), and neutrophil number of per 500 GMPs (E) were shown. (F) Erythrocyte-depleted BMCs of WT and Wip1KO mice were treated with G-CSF in the presence or absence of 10μM U0126 (inhibitor of ErK), 5μM SB203580 (inhibitor of p38), 10μM MTA (inhibitor of STAT1), and the transcriptional factor C/EBPα expression were detected by immunoblotting. (G) A total of 500 GMPs sorted from WT and Wip1KO mice were seeded in methylcellulose media supplemented with SCF, IL-3, and G-CSF in the presence or absence of U0126, SB203580, or MAT. The experiment was performed in triplicate. One CFU with a representative size generated from WT or Wip1KO GMPs was photographed. Absolute neutrophil number per CFU (H), number of CFUs (I), and neutrophil number of per 500 GMPs (J) were detected after 8 days in culture. Data (mean ± SD) are one of 2 independent experiments with similar results. *P < .05, between the indicated groups. **P < .01, between the indicated groups. ***P < .001 between the indicated groups.