Fig. 7

CCL5 increased growth cone formation through activating the mTOR and FAK pathway. A Phalloidin (red) labeled the filopodia in axon growth cones of WT or CCL5-KO neurons after treating with CCL5 (0, 100, 250, 500, 1000 pg/ml). Tuj-1 labeled neurites, and DAPI labeled the nucleus. Phalloidin labeled growth cones in different groups were enlarged in the boxed regions: scale bar = 50 μm and 5 μm. The fluorence intensity of Phalloidin and neurite branching in different groups was quantified in B, C. (B: KO neuron treated with CCL5, p = 0.027; WT vs. KO neuron, p < 0.0001). (C: WT neuron treated with CCL5, p = 0.0089; KO neuron treated with CCL5, p < 0.0001; WT contol vs. KO contol, p = 0.0009 by t-test). D The activation of p70s6k/mTOR, NRG-1, FAK, and Erk signaling proteins in neurons after treatment with CCL5 (0, 100, 250, 500, 1000 pg/ml) in westen blot analysis. FGF was taken as positive control. Quantification data were in E-H. E The activation of p70s6k by CCL5 p = 0.0182; the activation of p70s6k by FGF p = 0.0079. F The activation of mTOR by CCL5 p = 0.0217; the activation of mTOR by FGF p = 0.0169. G The activation of ERK1/2 by CCL5 p = 0.0437; the activation of ERK1/2 by FGF p = 0.0025. Data was analyzed by one-way ANOVA in same group and two-way ANOVA between groups. Data between control and FGF treatment was analyzed by t-test