Figure 8

FPRs-induced neuronal differentiation of NSCs was mediated by the PI3K-AKT signaling pathway. (A–H) FPR1-induced neuronal differentiation of NSCs was mediated by the PI3K-AKT signaling pathway. (A,B) Western blot analysis of AKT activity in NSCs with or without preadministering LY294002 for 30 min before administering fMLF. (A) Representative immunoblots. (B) Relative quantification for AKT activity. (C,D) Dissociated NSCs were differentiated with or without preadministering LY294002 for 30 min before administering fMLF. The images in (C) are representative of several independent experiments, and the graph in (D) shows the statistical results. (E) Representative immunoblots. (F) Histograms showing relative levels of β-III tubulin and GFAP. (G) Dissociated NSCs were differentiated in an extremely low density (1000 cells/mL), and then the cells were immunostained with β-III tubulin. (H) Quantified analysis of the total length of neurites per cell, the number of primary neurites, and the number of branch points. (I–P) FPR2-induced neuronal differentiation of NSCs was mediated by the PI3K-AKT signaling pathway. (I,J) Western blot analysis of AKT activity in NSCs with or without preadministering LY294002 for 30 min before administering MMK-1. (I) Representative immunoblots. (J) Relative quantification for AKT activity. (K,L) Dissociated NSCs were differentiated with or without preadministering LY294002 for 30 min before administering MMK-1. The images in (K) are representative of several independent experiments, and the graph in (L) shows the statistical results. (M) Representative immunoblots. (N) Histograms showing relative levels of β-III tubulin and GFAP. (O) Representative micrographs of the differentiated cells immunostained with β-III tubulin. (P) Quantified analysis of the total length of neurites per cell, the number of primary neurites, and the number of branch points. Data were presented as mean ± SEM. *P < 0.05; **P < 0.01; N = 4. Scale bar = 20 µm.