Fig. 2.

TR3/Nur77 expression and vascular permeability (A) Macroscopic images illustrate leakage of EB dye at 0.5, 1, and 3 d after implantation of Matrigel plugs with indicated contents of VEGF-A¹⁶⁵–secreting SKMEL/VEGF cells and PT67 cells packaging indicated cDNAs. Dye from 1- and 3-d time points was extracted and quantified (Fig. S1, eight animals per group). At 1 d, lanes 5 and 6 differed significantly from all other lanes (P < 0.001, Tukey–Kramer test); at 3 d, lanes 1 and 4 differed significantly from all other lanes (P < 0.001). (B) BVP, 30 min after intravenous EB dye injection, in selected organs of wild-type (Upper) and EC-Nur77-S mice (Lower), and AVH after VEGF-A¹⁶⁵ injection in flank skin. EB dye extravasation was quantified and, in all organs except uterus and brain, EC-Nur77-S was significantly greater than wild-type Fvb mice (P < 0.001 for mesentery, testis, lung, kidney, heart, and skin ± HBSS or VEGF-A¹⁶⁵; P < 0.01 for liver, Mann–Whitney test). (C) Liver and heart sections immunostained for CD31. Mother vessels that formed in EC-Nur77-S transgenic mice were significantly enlarged (P < 0.001), but vascular density vs. control wild-type mice was unchanged (P = 0.15) (unpaired t test). Four mice per group, based on three different transgenic founders. (D) EB dye leakage induced by HBSS or VEGF-A¹⁶⁵ in flank skin and mesentery was significantly greater in wild-type Fvb mice than in EC-Nur77-DN mice 6 d after withholding tetracycline (**P < 0.01, ***P < 0.001, unpaired t test).