Figure 5 | Experimental & Molecular Medicine

Figure 5

From: PPARγ modulates vascular smooth muscle cell phenotype via a protein kinase G-dependent pathway and reduces neointimal hyperplasia after vascular injury

Figure 5

The activation of PKG induced by rosiglitazone (RSG) is mediated not by a change in NO or cGMP but by the increased binding of Sp1 on the protein kinase G (PKG) promoter. (a–c) We tested the effect of RSG on the NO-cGMP-PKG pathway. RSG did not change the level of NO or cGMP. iNOS, inducible nitric oxide synthase, n=4. (d) Chromatin immunoprecipitation (ChIP) assay for the PKG promoter showed that the activation of PKG was induced by the increased binding of Sp1 on the promoter region of PKG. Moreover, mithramycin, a Sp1 inhibitor, reversed the increased binding activity of Sp1 induced by RSG. (e) Collectively, all these results suggest that the effect of RSG is exerted by the increase of Sp1-binding activity on the PKG promoter, not by regulating the level of NO or cGMP. GAPDH, glyceraldehyde 3-phosphate dehydrogenase; IP, immunoprecipitation; sGC, soluble guanylyl cyclase; V, vehicle; VASP, vasodilator-stimulated phosphoprotein; VSMC, vascular smooth muscle cell.

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