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. 2014 Mar 26;1:14004. doi: 10.1038/mtm.2014.4

Figure 1.

Figure 1

The effect of SNC-Fc mutation and truncation on vascular smooth muscle cell (VSMC) apoptosis. (a) Diagrammatic representation of the SNC-Fc molecule to show the locations of the fibroblast growth factor receptor (FGFR) and N-cadherin binding sites, the mutations to prevent binding, and truncation of SNC-Fc to EC4-Fc. (b,c) The percentage of apoptotic VSMCs (assessed by cleaved caspase-3 immunocytochemistry) 24 hours after induction of apoptosis with Fas-L and treatment with the purified proteins (mean ± SEM, n = 3, *P < 0.05 versus Fc, #P < 0.05 versus FGFR mutated, $P < 0.05 versus EC4 mutant). (d) EC4 activated Akt signaling to the same extent as SNC-Fc. Analysis of phospho-Akt immunocytochemistry following 24-hour treatment with the purified proteins (mean ± SEM, n = 4, *P < 0.05 versus Fc, FGFR mutated and EC4 mutant). EC, extracellular; SNC, soluble N-cadherin.