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Qun Zeng, Agustina Palacio, Ahmet Ozkok, Douglas K Sigford, Jian Cai, Shlomit Schaal, Tongalp H Tezel; PANRETINAL PHOTOCOAGULATION INDUCES AUTOANTIBODY PRODUCTION AGAINST RETINAL ANTIGENS. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4929.
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© ARVO (1962-2015); The Authors (2016-present)
To characterize the humoral response against retinal autoantigens after laser photocoagulation.
Serum samples were collected from 10 diabetic patients before and four weeks after initial panretinal photocoagulation. Collected serum samples were cross-blotted with human retinal protein extracts on a 2-dimensional gel. Retinal antigens recognized by patients’ serum were identified using LC-MS/MS. Similarly, laser 5 adult Brown Norway rats that were sacrificed two weeks after laser photocoagulation. Extracted retinal proteins were cross-blotted with pre- and post-laser serum samples. Retinal antigens were identified using mass spectroscopy.
Serum from untreated patients with proliferative diabetic retinopathy was positive 8 common autoantibodies against retinal proteins, i.e. carbonic anhydrase, glyceraldehyde-3-phosphate dehydrogenase, voltage-dependent anion-selective channel protein 1, creatine kinase B-type, alpha enolase, vimentin, pyruvate kinase and fructose-bisphosphate aldolase A. Laser photocoagulation boosted up antibody production against these proteins, as well as induced de novo antibodies against heat shock cognate 71 kDa protein, cellular retinoic acid-binding protein 1, tubulin beta, vimentin, aldolase, GFAP, aconitate hydratase and gamma-enolase. Antibodies against six of the identified retinal autoantigens (heat shock cognate 71 kDa protein, alpha enolase, creatine kinase B-type, glyceraldehyde-3-phosphate dehydrogenase, tubulin beta and pyruvate kinase) were also observed after the photocoagulation in the rat.
Humoral response to retinal autoantigens is common among untreated patients with proliferative diabetic retinopathy due to leaky blood-retinal barrier. Laser photocoagulation boosts up this humoral response and induces additional retinal autoantibodies. Some of these autoantibodies may reflect neuronal damage, i.e. glyceraldehyde-3-phosphate dehydrogenase, whereas other may explain retinal function loss in diabetes, (pyruvate kinase, carbonic anhydrase) and/or after panretinal photocoagulation (heat shock cognate 71 kDa protein, alpha enolase).
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