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. 2009 Dec 23;298(4):C952–C960. doi: 10.1152/ajpcell.00466.2009

Fig. 6.

Fig. 6.

MAPKs mediate the effect of thrombin on AP-1 activation in RAECs. A: RAECs were treated with thrombin (30 U/ml) for 0–30 min, and the abundance of phosphorylated (p) c-Jun and ATF-2 to total c-Jun and ATF-2 was evaluated by immunoblot analyses. Thrombin induced a transient phosphorylation of these two transcription factors. B: RAECs were treated with thrombin (30 U/ml) for 0–30 min, and the abundance of phosphorylated SAPK/JNK and p38 MAP kinase to total SAPK/JNK and p38 MAP kinase was evaluated by immunoblot analysis. C: RAECs were preincubated with DMSO, JNK inhibitor SP600125, or p38 MAPK inhibitor SB202190 for 0, 5, or 20 min. The abundance of phosphorylated c-Jun and ATF-2 to total c-Jun and ATF-2 was evaluated by immunoblot analysis. D: RAECs were incubated with thrombin (30 U/ml) and SB202190 for 4 h. The abundance of arginase I protein was assessed. Tubulin protein level was evaluated to serve as a loading control. Results shown are representative of three independent experiments.