Figure 2. Impaired vascular integrity in mice lacking FGF signaling.

(A) Increased vascular permeability and impaired endothelial morphology in sFGFR1IIIc mouse. Ten days after adenoviral injection in C57BL/6 mice, the trachea vasculature was stained for CD31 (red). Green represents microspheres in the extravascular space. Scale bars: 20 μm (left panels); 10 μm (right panels). (B) sFGFR1IIIc increases vascular permeability in the muscle. Ad-Null (control) or Ad-sFGFR was injected in C57BL/6 mice, and 14 days later, Evans blue dye was injected i.v. The adductor group muscles were harvested for quantitation. Data are shown as mean ± SD (n = 4). *P < 0.05, control vs. sFGFR1IIIc by t test. (C) Inhibition of FGF signaling in the heart and lung increases vascular permeability. Ad-Null (control), Ad-sFGFR was injected in C57BL/6 mice, and 10 days later, Evans blue dye levels were examined in the heart and lung. Data are shown as mean ± SD for n = 7, control; n = 8, sFGFR1IIIc; n = 4, sFGFR3IIIb; n = 4, sFGFR3IIIc. *P < 0.05, vs. control by t test. (D) Increased vascular permeability in Ad-sFGFR1IIIc–treated nude mouse. NU/NU nude mice (Charles River Laboratories) were subjected to trachea CD31. Junctional CD31 staining observed in control (arrows) is completely absent in the Ad-sFGFR1IIIc–treated trachea vasculature. Scale bars: 20 μm (left panels); 10 μm (right panels). (E) Hemorrhage observed in Ad-sFGFR1IIIc–treated mouse lung and heart. Ten days after adenoviral injection in nude mice, lung and heart were harvested for H&E staining. Upper panels show lung sections and lower panels show heart sections. Black arrows indicate myocardial hemorrhage. Original magnification, ×400.