In vitro effects of c(RGDf[NME]V) and RGDechiHCit on vascular smooth muscle cell (VSMC) cell proliferation (Panel A) and DNA synthesis assayed by [3H]thymidine incorporation (Panel B). In this cellular setting, hFN induced a mitogenic stimulus, appreciable especially at 20h. c(RGDf[NMe]V) but not RGDechiHCit at that time-point induced an attenuation of such proliferative response. All experiments were performed from three to five times in triplicate (* = p < 0.05 vs Basal; # = p < 0.05 vs hFN). In vitro effects of c(RGDf[NMe]V) and RGDechiHCit on VSMC signal transduction were represented in Panel C. Extracellular signal regulated kinase (ERK)/mitogen-activated protein kinase activation: western blot of activated (phosphorylated: pERK) ERK2 after hFN-stimulation. Blots were then stripped and reprobed for either total ERK as a loading control. Densitometric analysis (bar graph) showed that hFN induced ERK phosphorylation (* = p < 0.05 vs Basal) and that treatment with c(RGDf[NMe]V) but not RGDechiHCit decreased such activation (# = p < 0.05 vs hFN). Error bars show SEM. Representative blots are presented in the inset.