p120 Modulates LPS-Induced NF-κB Activation Partially through RhoA in Bronchial Epithelial Cells
Figure 6
p120 activates NF-κB signaling pathway partially through RhoA. (a) Coimmunoprecipitation confirmed the interaction of p120 and RhoA. The level of p120-bound RhoA was unchanged. (b) The expression of total RhoA also remained unchanged. (c) The relative level of active RhoA was increased dramatically from 30 min to 60 min by G-LISA analysis. Data were expressed as means ± SD (), versus control group (0 min). (d) LPS-induced NF-κB activation was inhibited by ROCK inhibitor Y27632. Cells were pretreated with Y27632 for 12 h before LPS stimulation (60 min). Nuclear translocation of NF-κB p65 was partially inhibited. Lamin B served as a nuclear marker, and β-actin served as a cytoplasmic marker. (e) RhoA activity was decreased in both exogenous p120 3A and p120 ΔN overexpression groups, compared with MT group after LPS treatment. Data were expressed as means ± SD (), versus MT + No-LPS, p120 ΔN + No-LPS, and p120 3A + No-LPS group, respectively. versus MT + LPS group. (f) The level of p120-bound RhoA could not be detected after p120 complete knockdown. (g) RhoA activity was sharply upregulated after p120 knockdown both with and without LPS treatment. Data were expressed as means ± SD (); versus scramble + No-LPS and siRNA + No-LPS, respectively. versus scramble.
