PURPOSE: To identify vitreous proteins that were differentially expressed in patients suffering from proliferative diabetic retinopathy with active neovascularization. METHODS: The vitreous samples of 15 active proliferative diabetic retinopathy patients were analyzed by two-dimensional gel electrophoresis and mass spectrometry, and the results were compared with those from age-matched patients with macular hole. RESULTS: Twenty-five protein spots were identified in the two-dimensional gel electrophoresis gels. Eight proteins (pigmented epithelium derived factor, serine protease inhibitor, apolipoprotein A-IV precursor, prostaglandin-H2 D-isomerase, a(1)-antitrypsin precursor, ankyrin repeat domain 15 protein, alpha2-HS-glycoprotein, and beta V spectrin) in the 25 spots were expressed significantly differently between the macular hole and proliferative diabetic retinopathy patients (p value < 0.05). Five proteins were upregulated in the proliferative diabetic retinopathy patients, and three were downregulated (p value < 0.05). CONCLUSIONS: We constructed vitreous protein profiles for proliferative diabetic retinopathy patients and identified eight candidate proteins believed to be involved in the pathogenesis of proliferative diabetic retinopathy.
PURPOSE: To identify vitreous proteins that were differentially expressed in patients suffering from proliferative diabetic retinopathy with active neovascularization. METHODS: The vitreous samples of 15 active proliferative diabetic retinopathypatients were analyzed by two-dimensional gel electrophoresis and mass spectrometry, and the results were compared with those from age-matched patients with macular hole. RESULTS: Twenty-five protein spots were identified in the two-dimensional gel electrophoresis gels. Eight proteins (pigmented epithelium derived factor, serine protease inhibitor, apolipoprotein A-IV precursor, prostaglandin-H2 D-isomerase, a(1)-antitrypsin precursor, ankyrin repeat domain 15 protein, alpha2-HS-glycoprotein, and beta V spectrin) in the 25 spots were expressed significantly differently between the macular hole and proliferative diabetic retinopathypatients (p value < 0.05). Five proteins were upregulated in the proliferative diabetic retinopathypatients, and three were downregulated (p value < 0.05). CONCLUSIONS: We constructed vitreous protein profiles for proliferative diabetic retinopathypatients and identified eight candidate proteins believed to be involved in the pathogenesis of proliferative diabetic retinopathy.
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