Figure 4.
HgCl2 activates the Jak2/STAT5 pathway to promote the differentiation of EMPs in B10.S mice. B10.S mice were treated with the control or 50 μM HgCl2 for 4 w, and multiple signaling molecules involved in erythropoiesis including PU.1, IRF1, p-Jak1, p-Jak2, p-STAT1, p-STAT3, and p-STAT5 were measured for EMPs in the BM thereafter; FACS-purified EMPs from the BM were treated in the presence or absence of inhibitors for the Jak2/STAT5 signaling pathway in vitro for 16 h to evaluate its impact on STAT5 signaling and EMP differentiation into BFU-Es, CFU-Es, and MkPs. (A) The expression of PU.1 (mean fluoresce intensity, MFI) in EMPs in the BM. (B) The expression of IRF1 (MFI) in EMPs in the BM. (C) The expression of p-Jak1 and p-Jak2 (MFI) in EMPs in the BM. (D) The expression of p-STAT1, p-STAT3, and p-STAT5 (MFI) in EMPs in the BM. (E) The expression of p-STAT5 (MFI) in EMPs in the presence or absence of Jak2 inhibitor (fedratinib) in vitro. (F) The number of BFU-Es in the in vitro assay. (G) The number of CFU-Es in the in vitro assay. (H) The number of MkPs in the in vitro assay. Each dot represents one mouse or one sample, and a total of 5 to 12 mice were used for each group. Asterisk indicates a significant difference compared to the counterpart control group. p < 0.05 was considered as the level of significant difference.