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. 2010 Dec 3;90(1):88–96. doi: 10.1093/cvr/cvq385

Figure 6.

Figure 6

Role of JNK and p38 on Rac1 and RhoA-mediated regulation of angiotensinogen gene expression. CFs were treated for 24 h with adenoviruses expressing constitutively active Rac1 (Rac1-CA) (A) and RhoA (RhoA-CA) (B). Cells were then treated for 1 h with p38 inhibitor (10 µM SB-203580) and JNK1/2 inhibitor (20 µM SP-60125) and cells were harvested for RNA. Expression of Ao mRNA was determined by real-time RT-PCR as described in the Methods. Both RhoA overexpression and JNK1/2 inhibition markedly increased the basal Ao gene expression. RhoA-CA-mediated basal activation of Ao gene expression was significantly reduced by p38 blockade. However, JNK1/2 inhibition-mediated basal activation of Ao is completely abrogated by overexpression of Rac1. Results are means ± SEM from four independent experiments. SB, SB-203580; SP, SP-60125; V, vehicle (0.05% DMSO).