April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
PANRETINAL PHOTOCOAGULATION INDUCES AUTOANTIBODY PRODUCTION AGAINST RETINAL ANTIGENS
Author Affiliations & Notes
  • Qun Zeng
    Ophthalmology & Vision Science, University of Louisville, Louisville, KY
  • Agustina Palacio
    Ophthalmology & Vision Science, University of Louisville, Louisville, KY
  • Ahmet Ozkok
    Ophthalmology & Vision Science, University of Louisville, Louisville, KY
  • Douglas K Sigford
    Ophthalmology & Vision Science, University of Louisville, Louisville, KY
  • Jian Cai
    Medicine, University of Louisville, Louisville, KY
  • Shlomit Schaal
    Ophthalmology & Vision Science, University of Louisville, Louisville, KY
  • Tongalp H Tezel
    Ophthalmology & Vision Science, University of Louisville, Louisville, KY
    Anatomy and Neurobiology, University of Louisville, Louisville, KY
  • Footnotes
    Commercial Relationships Qun Zeng, None; Agustina Palacio, None; Ahmet Ozkok, None; Douglas Sigford, None; Jian Cai, None; Shlomit Schaal, None; Tongalp Tezel, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 4929. doi:https://doi.org/
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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. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: To characterize the humoral response against retinal autoantigens after laser photocoagulation.

Methods: 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.

Results: 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.

Conclusions: 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).

Keywords: 499 diabetic retinopathy • 663 proteomics • 555 immunomodulation/immunoregulation  
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