Figure 2 | Experimental & Molecular Medicine

Figure 2

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

Figure 2

Rosiglitazone (RSG) modulates vascular smooth muscle cell (VSMC) phenotype through protein kinase G (PKG) activation. Immunofluorescence staining for calponin, α-smooth muscle actin (SMA) and thrombospondin. Calponin and α-SMA are markers of the differentiated contractile form of VSMCs. In contrast, thrombospondin is a marker of the synthetic form of VSMCs. (a, b) Platelet-derived growth factor (PDGF) treatment reduced calponin and α-SMA levels. RSG treatment prevented the change in each marker induced by PDGF treatment. PKG inhibitor reversed the effect of RSG, suggesting that RSG modulated VSMC phenotype through PKG activation. Scale bar=10 μm. (c) The opposite effect was observed for thrombospondin.

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