JAM-1 is involved in bFGF-induced angiogenesis. (A) Serum-starved untransfected HUVECs were plated on vitronectin and stained to observe cellular morphology. bFGF-treated cells (ii) formed cellular extensions (arrows) that were blocked by anti–JAM-1 antibody (iii). (B) Low-power light micrograph of representative CAMs. (i-ii) CAM treated with PBS (control) or stimulated with 50 ng/mL bFGF. (iii-iv) bFGF-stimulated CAM was treated topically with anti-αvβ3 (2.5 μg/mL) or anti–JAM-1 (5 μg/mL) antibodies. (C) Angiogenic index of the data obtained from anti–JAM-1-treated CAMs shows dose-dependent inhibition of bFGF-induced angiogenesis (n = 8 CAMs; *P < .05). Index values were normalized by subtracting control (PBS) values. (D) Low-power light micrograph of representative murine aortic ring assay. (i) bFGF; (ii) bFGF+clgG; (iii) bFGF+anti-JAM1. (iv) Graph represents the number of microvessel sprouts per field. Anti–JAM-1 (10 μg/mL) significantly (*P < .005) inhibits bFGF-induced microvessel outgrowth (n = 6 mice). Original magnifications × 400 (A) and × 50 (B, D).
