Fig. 4
IGFBPs secreting PD-MSCsPRL-1 inhibit adipogenesis via upregulation of FAK and downregulation of the PI3K/AKT/mTOR signaling pathway. a Protein expression of PPAR-γ, Leptin, and TNF-α in normal and GO-derived OFs (GO-OFs) cocultured with naïve PD-MSCs (Naïve (+)) and PD-MSCsPRL-1 (PRL-1 (+)) for 24 h was analyzed using western blotting. Quantitative analysis of b PPAR-γ c Leptin and d TNF-α expression in normal and GO-OFs cocultured with naïve PD-MSCs and PD-MSCsPRL-1 for 24 h (mean ± SD *p < 0.05 compared with the noncoculture (−) groups) (mean ± SD #p < 0.05 compared with the naïve coculture groups). e Protein expression of phosphorylated (p-) and total (t-) PI3K, AKT, mTOR, and FAK in normal and GO-OFs cocultured with naïve PD-MSCs and PD-MSCsPRL-1 for 24 h was measured using western blotting. mRNA expression of f ITGA4, g ITGB7, and h FAK in normal and GO-OFs cocultured with naïve PD-MSCs and PD-MSCsPRL-1 for 24 h (mean ± SD *p < 0.05 compared with the noncoculture groups) (mean ± SD #p < 0.05 compared with the naïve coculture groups; individual open circle). Statistic significances were determined by nonparametric Kruskal-Wallis test