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P. N. Bishop, M. M. Le Goff, G. Ferris, D. Ruiz Nivia, S. P. Henry, M. Takanosu, R. Mayne; Opticin Inhibits Angiogenesis in the Oxygen-Induced Retinopathy Model. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1748.
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To determine whether the vitreous glycoprotein opticin has an inhibitory effect upon experimentally-induced preretinal neovascularisation.
Opticin null mice were generated and bred onto a C57/BL6 background through ten generations. The opticin null mice or wild-type controls were placed in 75% oxygen from P7-12 and then brought back to normoxia. At day P17 the eyes were fixed, wax embedded and sections were stained with haematoxylin and eosin. The sections were analysed to determine the number of neovascular nuclei per section on the vitreal side of the ILM. In a separate set of experiments wild-type mice were exposure to 75% oxygen between P7-12 and then at P14 one eye was injected intravitreally with opticin (2.5 µg in 1µ1 of PBS) and the contralateral eye with PBS alone. The eyes were analysed at P17 as above.
No morphological abnormalities were observed in the eyes of opticin null mice not exposed to hyperoxia. The opticin null mice that were exposed to high oxygen between P7-12 had an increased number of preretinal neovascular nuclei per cross section (109 +/- 5.6 S.E) compared to wild-type controls (73 +/- 2.9) (P < 0.001). The opticin injected wild-type eyes showed a decrease in preretinal neovascular nuclei per cross-section (38 +/- 3.1) compared to eyes injected with PBS alone (76 +/- 4.4) (P < 0.001).
A lack of opticin results in an increase in preretinal neovascularisation, whereas an excess of opticin results in a decrease in preretinal neovascularisation compared to controls. Therefore the levels of opticin in the vitreous may determine the susceptibility of patients to conditions such as proliferative diabetic retinopathy. Opticin could be used therapeutically to treat pathological angiogenesis.
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