Figure 5

Activation of the MAPK signaling pathway in E2-mediated odonto/osteogenic differentiation of SCAP. (A) SCAP were stained positively for ER-α. (B) Human breast carcinoma tissue served as a positive control. (C) PBS served as a negative control. Scale bars = 100 μm. (D) ER-α level detection by western blot analysis in control and E2-treated SCAP. (E) Quantitative analysis of the expression of ER-α in control and E2-treated SCAP. Values are mean ± SD, n = 3. **P <0.01. (F) The expression of MAPK related proteins (ERK, p-ERK, JNK, p-JNK, p38 and p-p38) by western blot. β-ACTIN was used as the internal control. (G) The ratio changes of p-ERK/ERK intensity in E2-treated SCAP. (H) The ratio changes of p-JNK/JNK intensity in E2-treated SCAP. (I) The ratio changes of p-p38/p38 intensity in E2-treated SCAP. (J) The expression of nuclear downstream transcription factors (Sp1, p-Sp1, Elk-1, p-Elk-1, c-Jun, p-c-Jun, c-Fos and p-c-Fos) by western blot analysis. (K) The ratio changes of p-Sp1/Sp1 intensity in E2-treated SCAP. (L) The ratio changes of p-Elk-1/Elk-1 intensity in E2-treated SCAP. (M) The ratio changes of p-c-Jun/c-Jun intensity in E2-treated SCAP. (N) The ratio changes of p-c-Fos/c-Fos intensity in E2-treated SCAP. Values are the mean ± SD, n = 3. *P <0.05, **P <0.01. ERα, estrogen receptor α; E2, 17beta estradiol; MAPK, mitogen-activated protein kinase; SCAP, stem cells from apical papilla; SD, standard deviation.