Fig. 6

Loss of CRP2 attenuates Ang II-induced Erk1/2 activation. A VSMCs were treated with 10 µmole/L Ang II and total proteins prepared at different time points for Western blot analysis to detect phosphorylated and total Erk1/2, and α-tubulin as a loading control. B Left panel, Apoe^−/− and Csrp2^−/−Apoe^−/− VSMCs were stimulated with Ang II and proteins harvested at 0, 10, and 30 min for Western blot analysis to detect phosphorylated and total Erk1/2, CRP2, and α-tubulin. A representative of 4 independent experiments is shown. Right panel, Quantitation of phospho-Erk1/2. Phosphorylated Erk1/2 level from Apoe^−/− VSMCs without Ang II treatment was set as 1. ^§P < 0.05 compared with the respective baseline without Ang II; *P < 0.05 compared with the corresponding Apoe^−/− group. C Apoe^−/− and Csrp2^−/−Apoe^−/− VSMCs were stimulated with Ang II and proteins harvested at 6, 12, and 24 h for Western blot analysis. D Left panel, Csrp2^−/−Apoe^−/− VSMCs were transfected with pMyc-His vector or pMyc-His-CRP2 plasmid and treated with Ang II. Total proteins were then harvested at 0, 10, and 30 min for Western blot analysis to detect phosphorylated and total Erk1/2, CRP2, and Myc. A representative of 3 independent experiments is shown. Right panel, Quantitation of phospho-Erk1/2. Phosphorylated Erk1/2 level from pMyc-His-vector-transfected VSMCs at time 0 was set as 1. ^§P < 0.05 compared with the respective baseline without Ang II; *P < 0.05 compared with the corresponding vector group