Fig. 6.

The inhibitory effect of CCL5 on Ang II-induced VSMCs proliferation is mediated by the AT₂ receptor. (A, B) SHR VSMCs were treated with Ang II (0.1 µmol/l) and/or CCL5 (100 ng/ml) in the presence or absence of losartan (AT₁ receptor antagonist, 10 µmol/l, A) or PD123,319 (AT₂ receptor antagonist, 10 µmol/l, B) for 24 h in medium containing [³H]-thymidine (1 µCi/ml). [³H]-thymidine incorporation is shown on the Y-axis. Bars represent means±SD from three independent experiments. ^ap <0.05 vs. VSMCs treated with Ang II. ^bp <0.05 vs. VSMCs treated with CCL5. ^*p<0.05 vs. VSMCs treated with Ang II/CCL5. (C) SHR VSMCs were plated on 24-well plates, grown to 90% confluence and then transfected with AT₂ receptor siRNA oligomers (50 nmol/l). VSMCs were then untreated or treated Ang II (0.1 µmol/l) and/or CCL5 (100 ng/ml) for 24 h in medium containing [³H]-thymidine (1 µCi/ml). [³H]-thymidine incorporation is shown on the Y-axis. Bars represent means±SD from three independent experiments.