Fig. 4

The high level of E₂ induces overproliferation of endometrium via FGF-FGFR-ERK signaling cascade. A Immunohistochemical analysis of PCNA in endometrial explants treated with or without recombinant FGF7. Scale bar: 20 μm. B Western blotting analysis of PCNA in endometrial explants treated with or without recombinant FGF7 (n = 7). The upper panel shows the quantification of PCNA level. C and D Western blotting analysis of phosphorylation levels of FGFR (C) and ERK (D) in endometrial explants treated with or without recombinant FGF7 (n = 7). The upper panels show the quantification of pFGFR and pERK levels. E and F Western blotting analysis of phosphorylation levels of FGFR (E) and ERK (F) in endometrial explants treated with the high level of E₂ alone or in combination with FGFR inhibitor (n = 5). The upper panels show the quantification of pFGFR and pERK levels. G Western blotting analysis of phosphorylation levels of ERK in endometrial explants treated with the high level of E₂ alone or in combination with ERK inhibitor. The upper panel shows the quantification of the pERK level (n = 5). H Immunohistochemical analysis of PCNA in endometrial explants treated with or without FGFR inhibitor or ERK inhibitor. Scale bar: 20 μm. I Western blotting analysis of PCNA in endometrial explants treated with or without FGFR inhibitor or ERK inhibitor (n = 5). The upper panel shows the quantification of PCNA level. Data are presented as the mean ± SEM. ^*P < 0.05, ^**P < 0.01. PCNA, proliferating cell nuclear antigen; FGF7, fibroblast growth factor 7; FGFR, fibroblast growth factor receptor; ERK, extracellular signal-regulated kinase; pFGFR, phosphorylated FGFR; pERK, phosphorylated ERK; E₂, estradiol