Fig. 4: Increased Akt signaling activity abolishes the FSH-induced inhibitory effects on various endometrial stem cell functions.

A schematic summary of the role of the PI3K/Akt signaling pathway in mediating the FSH-induced inhibitory effects on endometrial stem cells is described (a). Endometrial stem cells were prestimulated with the Akt activator SC79 (10 µM) for 1 h prior to FSH (30 IU/ml) treatment for 48 h. The FSH-induced effects on cell growth were then analyzed by MTT assays (b). The attenuating effects of the Akt activator on FSH-induced migration abilities were measured by Transwell assays (c) and western blotting for the cell migration regulators MMP-2 and MMP-9 (d). Endometrial stem cells were prestimulated with the Akt activator SC79 (10 µM) for 1 h prior to an additional FSH (30 IU/ml) treatment for 48 h. The effects on adipogenic and osteogenic differentiation capacity were then analyzed by oil red O and alizarin red S staining, respectively. Relative quantification of calcium deposition and lipid droplet (LD) secretion from differentiating cells was performed by measuring the absorbance of solubilized cells at 500 nm and 570 nm, respectively (e). β-Actin was used as an internal control. All experiments were performed in triplicate. Data are presented as the mean ± standard deviation (SD). *p < 0.05; **p < 0.005; and ***p < 0.001 (two-sample t test).