Fig. 2

Au-NP treatment rapidly changed the phosphorylating status of FAK, AKT and ERK, and subsequently contributing to Au-NP-mediated AQP1 accumulation. bEnd.3 cells were incubated with 500 ng/mL Au-NPs for 15, 30 and 60 min, and the phosphorylating status of FAK, AKT, ERK, and Cav1 was measured by western blots. a Representative images showed an augmentation of FAK and AKT phosphorylation; a reduction of ERK and Cav1 phosphorylation in Au-NP-treated groups in time-dependent manner, as compared to control. Also, Au-NP treatment caused an accumulation of Cav1 protein level. Quantified data was gained by densitometry analysis, followed by a normalized process to their total form. b phospho-FAK, (c) phospho-AKT, (d) phospho-ERK, (e) Cav1 and (f) phospho-Cav1. (* p < 0.05, ** p < 0.01, and *** p < 0.001 indicates statistically significant difference from the control group; N > 10). g Cells were pre-incubated with 10 μM U0126 (ERK inhibitor), 10 μM GDC-0068 (pan-AKT inhibitor) and 10 μM PF-573228 (FAK inhibitor), subjected to a 12–16 h exposure of Au-NPs. Images and quantified data revealed that Au-NP-induced AQP1 expression was prevented while FAK and AKT inhibition, whereas an enhancement of AQP1 expression was presented in the presence of U0126. (* p < 0.05, ** p < 0.01, and *** p < 0.001 indicates statistically significant difference from the control group; ## p < 0.01, and ### p < 0.0001 indicates statistically significant difference from the Au-NP-treated group; N = 7)