FIGURE 7.
Redoxosomal ROS induced by SOD1G93A augments TNFα production and NFκB activation in glial cells, whereas alsin attenuates these end points by inhibiting SOD1G93A-induced Rac1 activation. A and B, mouse glial cells were infected with Ad.SOD1G93A and treated with 0.1 mg/ml of SOD and 0.1 mg/ml of catalase proteins at 18 h post-infection. Cells were then infected with Ad.NFκBLuc at 24 h. At 48 h post-Ad.SOD1G93A infection, culture medium and cells were harvested separately and concentrations of TNFα in the media were determined (A) and NFκB activity in the cells was assayed (B). C, mouse glial cells were infected with the indicated vectors for 36 h prior to collection of the cells for Rac1 activity assays. D, mouse glial cells were infected with Ad.Alsin plus the vectors indicated for 36 h prior to obtaining 100,000 ×g endomembrane pellets. These samples were then used for Western blotting for alsin (top panel). The intensity of the alsin bands was quantified (bottom panel). Data represent the mean ± S.E. with n = 3; marked comparisons (*, #, or ∧) demonstrate significant differences from one-way analysis of variance followed by Student's t test of the comparisons (p < 0.05).