[Expression and role of endostatin in the retina of oxygen-induced retinopathy mouse model]

To investigate the effect of endostatin on the pathogenesis and development of retinal neovascula animal model of oxygen-induced retinopathy.

The animal model of oxygen-induced retinopathy was made by subjecting postnatal mice to hyperoxic conditions (5 days) followed by normoxic conditions. Retinal angiogram was taken by using high molecular weight fluorescein-dextran. The degree of hyperoxia-induced neovascularization in serial paraffin cross-sections was quantified by counting the number of vascular cell nuclei on vitreal side of the internal limiting membrane. The expression of ES and VEGF in the oxygen-induced retina was observed by immunohistochemistry.

We successfully constructed the oxygen-induced retinopathy mouse model. FITC-dextran retinal angiography indicated that hyperoxia could produce constriction of retinal vasculature and vaso-obliteration or irreversible closure of many capillary channels and eventually result in non-perfused area in the post-area of retina surrounding the optic disk. Relatively, hypoxia could lead to dilation and torsion of retinal vessels. There were averagely 22 neovascular nuclei per cross-section of eyes in the hyperoxia group and less than 3 nuclei per cross-section of eyes in the control group (P < 0.05). The expressions of ES and VEGF in the retina under hyperoxia were stronger than those under normoxia, expecially the expression of VEGF.

Taking measures to up-regulate the expression of endogenetic endostatin may have the potential for effective treatment of retinal ischemic neovascularization.