Purchase this article with an account.
SF Hackett, K Takahashi, Y Oshima, SJ Wiegand, GD Yankopoulos, PA Campochiaro; Angiopoietin 2 (Ang2) Plays an Important Role in Ocular Neovascularization (NV) . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1276.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Purpose: Mice deficient in Ang2 show lack of regression of the hyaloid vasculature and abnormal retinal vascular development. In this study, we used Ang2-deficient mice to explore the role of Ang2 in ocular neovascularization. Methods: Ang2-deficient mice and littermate controls were compared in 3 models of ocular NV, oxygen-induced ischemic retinopathy (OIR), ectopic expression of VEGF in photoreceptors (rho/VEGF transgenic mice), and choroidal NV (CNV) due to laser-induced rupture of Bruch's membrane. Results: In the OIR model, exposure of Ang2-deficient mice to high levels of oxygen resulted in partial regression of the already somewhat sparse retinal vessels. When these oxygen-exposed mice with few retinal vessels were moved to room air, there was no ischemia-induced retinal NV, while littermate controls developed extensive retinal NV. Mice deficient in Ang2 were crossed with rho/VEGF transgenic mice and F1 ang +/- mice that carried a rho/VEGF transgene were crossed with ang +/- mice. At P21, ang +/-offspring that carried a rho/VEGF transgene had extensive NV, while ang -/- mice that carried a rho/VEGF transgene had little evidence of NV. Two weeks after laser-induced rupture of Bruch's membrane, ang +/- mice developed prominent CNV, while ang -/- littermates had little or no CNV. Conclusions: Mice deficient in Ang2 develop little or no NV in 3 different models of ocular NV. These data suggest that Ang2 plays an important role in the development of pathologic NV.
This PDF is available to Subscribers Only