Figure 4

Effects of Exisulind mediated through PKG pathway in vitro and in vivo.

(A,B) The graphs show that PKG inhibitor (8-Rp-cPT-cGMP: 20 μM) reversed the effects of Exisulind on VSMCs viability and apoptosis. Exi = Exisulind. *P = 0.02 vs. PDGF group in (A), *P = 0.04 vs. vehicle group in (B). The data are presented as mean + SEM of five independent experiments. (C) Western blot assay demonstrates that the increased activity of PKG was reversed by PKG inhibitor (8-Rp-cPT-cGMP: 20 μM) treatment. p-VASP239 = phospho-VASP at serine239, t-VASP = total VASP, Exi = Exisulind. (D) In vivo sections at 2 weeks after injury demonstrated that the transfer of retroviral vector expressing active form of PKG (PKG IαS65D and PKG IßS80D) showed the similar effect of Exisulind-treated group, which was reversed by the transfer of retroviral vector expressing dominant-negative form of PKG (PKG IαK390R and IßK405R). Scale bar = 100 or 50 μm. In case of intimal area, *P = 0.02 vs. Mock (retroviral vector only expressing CMV promoter and green fluorescent protein, GFP) in control group, **P < 0.01 vs. Mock in Exisulind-treated group. In case of I/M ratio, *P = 0.04 vs. Mock (retroviral vector only expressing CMV promoter and green fluorescent protein, GFP) in control group, **P < 0.01 vs. Mock in Exisulind-treated group, n = 10 in each group.