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R.A. Samul, J. Shen, J. Zimmer, H. Liu, P.A. Campochiaro; Reduced Retinal Neovascularization (NV) in Neuropilin–2–deficient Mice . Invest. Ophthalmol. Vis. Sci. 2004;45(13):497.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Neuropilin–1 (Npn–1) and Npn–2 are receptors for semaphorins and function in axon guidance. They also act as coreceptors for particular isoforms of VEGF. There is evidence that Npn–1 plays an important role in embryonic vascular development and postnatal NV, but evidence regarding such a role for Npn–2 is lacking. In this study we used Npn–2 knockout mice (Npn2–/–) to explore the role of Npn–2 in retinal NV. Methods: In P15 Npn2+/+ mice with oxygen–induced ischemic retinopathy (OIR), retinal Npn–2 mRNA expression was measured by real–time RT–PCR and immuno–histochemistry for Npn–2 was performed on ocular frozen sections. The area of retinal NV was measured by image analysis of Griffonia simplicifolia lectin–stained ocular sections at P17 in Npn2–/– and Npn2+/+ mice with OIR. Npn2+/– mice were crossed with transgenic mice with VEGF expression in photoreceptors (V6, rho/VEGF mice) and V6/Npn2+/– were crossed. NV was measured in masked fashion in V6/Npn2–/– and V6/Npn2+/– mice. Results: At P15, mice with OIR had significantly more Npn–2 mRNA in the retina than control mice (2365±1062 vs. 939±650 copies/100,000 copies of cyclophilin A, p<0.0081). Immunohistochemistry localized Npn–2 to areas of NV. In the OIR model, there was a significant reduction in the area of retinal NV in Npn2–/– mice compared to wild type mice (0.00311±0.00049 vs. 0.0151±0.00233, p<0.01). V6/Npn2–/– mice had less retinal NV than V6/Npn2+/– mice (0.012265±0.009916 vs. 0.021276878±0.016222, p=0.029). Conclusions: These data suggest that Npn2 plays an important role in the development and modulation of retinal NV.
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