Skip to main content
. 2008 Sep 11;295(5):C1292–C1301. doi: 10.1152/ajpcell.00230.2008

Fig. 3.

Fig. 3.

Effect of CYP inhibition and EET antagonism on VEGF-induced endothelial cell tube formation and receptor phosphorylation. A: endothelial cell tube formation on fibronectin-coated culture dishes was assessed after 48 h in response to VEGF (30 ng/ml) or bFGF (30 ng/ml) in the absence and presence of solvent (Sol; DMSO, 0.01%), the EET antagonist 14,15-epoxyeicosa-5(Z)-enoicacid (EEZE, 10 μmol/l), or the CYP2C inhibitor N-methylsulfonyl-6-(2-propargyloxyphenyl)-hexanamide (MS-PPOH) (MS, 10 μmol/l). Representative photographs show the effect of VEGF in the absence and presence of MS-PPOH and EEZE. Bar graph summarizes data obtained in 3–7 independent experiments. *P < 0.05, **P < 0.01 vs. Sol. B: lack of effect of EEZE on the VEGF (30 ng/ml, 20 min)-induced phosphorylation of the VEGFR2 receptor in phospho-tyrosine immunoprecipitates (IP) from VEGFR2 overexpressing porcine endothelial cells.