Figure 6.

OIR-induced plus disease is dependent on ADAMs. The contribution of ADAMs to the development of vascular tortuosity following OIR was evaluated in Adam8^−/− and Adam9^−/− knockout mice, as well as in conditional knockout mice lacking ADAM10 or ADAM17 in endothelial cells (Adam10ΔEC or Adam17ΔEC mice), with wild-type littermates serving as controls. All animals were exposed to the OIR model and the retinas evaluated for vascular tortuosity at P17, as described in Materials and Methods. Adam8^−/− ([A]: n = 16; controls, n = 16) and Adam9^−/− ([B]: n = 8; controls, n = 8) mice, as well as Adam10ΔEC mice ([C]: n = 8; controls, n = 9), had significantly less vascular tortuosity than their wild-type controls. The Adam17ΔEC mice ([D]: n = 8; controls, n = 14) mice, however, did not display significant changes in their vascular tortuosity level after OIR. The vaso-obliteration and tuft formation were evaluated in the ADAM knockout mice as well their corresponding littermate controls ([E]; these results are taken from the original publications on the analysis of pathological retinal neovascularization in these animals, see Refs. 17–20 for details). Data represent average ± SEM; P values were determined using Student's t-test, *P ≤ 0.05.