Figure 2
In vitro effects of c(RGDf[NMe]V) and RGDechiHCit on cell proliferation (Panel A) and DNA synthesis assessed by [3H]thymidine incorporation (Panel B) in bovine aortic endothelial cells (EC). Given alone, c(RGDf[NMe]V) or RGDechiHCit did not affect EC proliferation. Neverteless, incubation with these αVβ3 integrin antagonists inhibited in a comparable way EC proliferation in response to the mitogenic stimulus, hFN. All experiments depicted in this figure were performed from three to six times in duplicate (* = p < 0.05 vs Basal, # = p < 0.05 vs hFN). Panel C. In vitro effects of c(RGDf[NMe]V) and RGDechiHCit on EC signal transduction. Extracellular signal regulated kinase (ERK)/mitogen-activated protein kinase activation: western blot of activated (phosphorylated: pERK) ERK2 after hFN-stimulation. Equal amounts of proteins were confirmed via blotting for total ERK. Densitometric analysis (bar graph) showed that hFN stimulation caused ERK activation (* = p < 0.05 vs Basal) and that treatment with αVβ3 antagonists blunted such activation (# = p < 0.05 vs hFN). Error bars show SEM. Representative blots are shown in the inset.