Figure 8.

Inhibition of JAM-C decreases microvascular permeability in vivo and hypoxia-induced retina angiogenesis. (A) Skin permeability (as assessed by leakage of Evans blue) induced by intradermal injection of VEGF or compound 48/80 is shown without (open bars) or with pretreatment with smJAM-C (gray bars). The control 6xHis peptide did not affect VEGF- or histamine-induced permeability. Permeability is shown as the percentage of control, defined as the skin permeability after intradermal injection with buffer in the absence of competitors, and data are shown as mean ± SD (n = 5 mice). (B and C) Mice were subjected to the ROP model. (B) The permeability of the retina was assessed by the leakage of Evans blue on day p13. 6 h before assessing the leakage of Evans blue, mice were treated i.p. with buffer, the control 6xHis peptide, or smJAM-C. The leakage of Evans blue was quantified as absorbance/dry weight of the retina, and data are represented as the percentage of control (buffer-treated mice) and are mean ± SD (n = 5 mice). (C) Retinal neovascularization was quantified on day p17 as described in Materials and methods. Mice were treated from day p12 until day p16 once daily i.p. with buffer, the control 6xHis peptide, or smJAM-C. Retinal neovascularization is presented as the percentage of control, defined as neovascularization in the presence of buffer only. Data are mean ± SD (n = 5 mice). *, P < 0.05; ns, not significant.